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Wednesday, October 31, 2012

Nephritis

Nephritis is defined as a condition of inflammation of the nephrons in the kidneys.

Types of Nephritis
Depending to the locations of inflammation, Nephritis can be classified as follows
I. Glomerulonephritis 
 Glomerulonephritis is defined as the condition of inflammation of the tiny filters in  kidneys (glomeruli), which filter blood by removing excess fluid, electrolytes and waste and pass them through urination.
1.. Acute Glomerulonephritis
A sudden onset of inflammation of glomeruli.
2. Chronic Glomerulonephritis
This is a graduated progression of kidney diseases. It can be primary or as a result of certain diseases 

II. Interstitial nephritis (Tubulo-interstitial nephritis) 
Interstitial nephritis is defined as a condition of inflammation of the spaces between renal tubules, affecting the interstitium of the kidneys and kidney function in wast removal.
1,  Acute Interstitial nephritis
A sudden onset of the inflammation of the diseases
2. Chronic Interstitial nephritis
In most case, it ends in kidney failure

I. Glomerulonephritis 
Glomerulonephritis is defined as the condition of inflammation of the tiny filters in  kidneys (glomeruli), which filter blood by removing excess fluid, electrolytes and waste and pass them through urination.
A. Signs and Symptoms
A.1. Acute Glomerulonephritis 
According to the study by Movchan EA, in the study of Evolutionary trends in symptoms of acute glomerulonephritis in adult population of the Novosibirsk region, indicated that AGN occurs not often but with stable rate. It is encountered more frequently in young men. The last decade is characterized by higher morbidity after streptococcal infection, high percentage of women at reproductive age, aggravation of the clinical course with marked edemas, severe arterial hypertension, renal dysfunction (acute renal failure in 10.4%), cases of left ventricular failure (5.2%) and eclampsia (1.7%) not registered earlier(1).

A.2. Chronic Glomerulonephritis 
In the study of Incidence and characteristics of the hypertension syndrome in chronic glomerulonephritis, by Dr. Stefanov G. showed that in the random group, 65.1 per cent had renoparenchymal hypertension (RPH), 34.8 per cent of the patients had RPH among the patients with normal renal function, and with various degrees of chronic renal insufficiency (ChRI) - 95.4 per cent..... In 48 per cent but patients with ChGN without RPH also had the same complaints--26 per cent. Complaints as dizziness, tinnitus and insomnia were rare. The hypertension was with a short duration (according to anamnestic data)--in 2/3 less than three years and 40 per cent of the patients had hypertonic crises or/and acute left cardiac insufficiency in spite of the relatively little alterations in ECG and fundus of the eye(2).

3. Other symptoms include 
a. Hematuria
Hematuria is condition of the presence of red blood cells in the urine.
There is a report of a a 16 year old male with a history of recurrent synpharyngitic macroscopic hematuria presented with severe loin pain, macroscopic hematuria and oliguric acute renal failure, according to the study by Dr. Kincaid-Smith P and the research team(3).

b. Proteinuria (The presence of an excess of proteins in the urine)
Proteinuria is the most important predictor of outcome in glomerulonephritis and experimental data suggest that the tubular cell response to proteinuria is an important determinant of progressive fibrosis in the kidney(4)

c. Cold sweating, general fatigue, and somnolence
  There is a report of a 66-year-old woman, who has been under hemodialysis due to antineutrophil cytoplasm autoantibody (ANCA)-associated glomerulonephritis since 2003, was hospitalized because of cold sweating, general fatigue, and somnolence, According to the research team at the Divisions of Endocrinology and Metabolism(5).

B. Causes and Risk factors
B.1. Causes
1. Infections
In the study of Glomerulonephritis causing acute renal failure during the course of bacterial infections of of four male patients, aged 53-71 years, who developed GN and ARF following bacterial infections, showed that
a. The first two patients developed GN with immunoglobulin A (IgA) deposits after infections with hospital-acquired methicillin resistant Staphylococcus aureus (MRSA). Clinical, serologic and histological features, classification of GN and treatment differed between the two patients.
b. The third patient developed simultaneous acute rheumatic fever and post-streptococcal GN causing severe ARF requiring hemodialysis. Complete recovery of ARF and migratory polyarthritis followed initiation of corticosteroids.
c. The fourth patient developed ARF and cerebral vasculitis following a prolonged course of Streptococcus mutans endocarditis with delayed diagnosis. He also developed multiple serological abnormalities including elevated titers of antineutrophil cytoplasmic antibodies (ANCA), antinuclear antibodies (ANA), anti-phospholipid antibodies, rheumatoid factor, and modest hypocomplementemia(6).

2. Lupus
In the study of Distinct roles for complement in glomerulonephritis and atherosclerosis revealed in mice with a combination of lupus and hyperlipidemia by Dr. Lewis MJ and the research team at the Imperial College London showed that accelerated atherosclerosis and renal inflammation in SLE are closely linked via immune complex formation and systemic complement depletion. However, whereas hyperlipidemia will enhance renal immune complex-mediated complement activation and the development of nephritis, accelerated atherosclerosis is, instead, related to complement depletion and a reduction in the uptake of apoptotic/necrotic debris(7).

3. Goodpasture's disease
In the study of the Progression from Goodpasture's disease to membranous glomerulonephritis, according to the research team at the Department of Renal Medicine, Concord Hospital, Sydney, thwew is report of an unusual case of a patient with Goodpasture's disease presenting with hemoptysis, severe iron deficiency anemia and microscopic hematuria and proteinuria.... Nine months after presentation he developed nephrotic range proteinuria and a repeat renal biopsy revealed membranous glomerulonephritis with no evidence of his original disease(8).

4.  IgA nephropathy
IgA nephropathy is an autoimmune disease, affecting the kidneys
IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23(9).

5. Polyarteritis nodosa (PAN)
Polyarteritis nodosa (PAN) is defined as a vasculitis of medium & small-sized arteries
There is a report of a 53-year-old man with hepatitis C virus (HCV) infection underwent cholecystectomy for presumed cholecystitis. Gallstones were not present, and histological examination demonstrated medium-sized arteritis, consistent with polyarteritis nodosa (PAN). The patient later developed rapidly progressive glomerulonephritis. Kidney biopsy demonstrated cryoglobulinemic glomerulonephritis(10).

6. Polyangiitis (Wegener's granulomatosis)
Polyangiitis is defined as a vasculitis of small-sized blood vessels. Granulomatosis with polyangiitis (GPA), is the recently proposed, new alternative name for Wegener's granulomatosis. It defines a systemic small-vessels vasculitis, characterized by frequent involvement of upper and lower respiratory tract. According to Dr. Karras A, and the research team at hôpital Européen Georges-Pompidou, service de néphrologie(11).

7. Other causes
a. Homozygous C1q deficiency
According to the study of in mice, Dr. Botto M and the research team at the Imperial College School of Medicine, indicated that among mice without glomerulonephritis, there were significantly greater numbers of glomerular apoptotic bodies in C1q-deficient mice compared with controls. The phenotype associated with C1q deficiency was modified by background genes. These findings are compatible with the hypothesis that C1q deficiency causes autoimmunity by impairment of the clearance of apoptotic cells(12).

b.  Deficiency of factor H
Factor H is a member of the regulators of complement activation family, a complement control protein. Factor H, the main regulator of this activation, prevents formation and promotes dissociation of the C3 convertase enzyme, and, together with factor I, mediates the proteolytic inactivation of C3b. Factor H deficiency, described in 29 individuals from 12 families and in pigs, allows unhindered activation of fluid-phase C3 and severe depletion of plasma C3 (ref. 11). Membranoproliferative glomerulonephritis (MPGN) occurs in factor H-deficient humans and pigs(13).
 
B.2. Risk factors
1. Age, hypertension, and presence of nephrotic range proteinuria
The risk factors for renal dysfunction were the age, hypertension, and nephrotic range proteinuria during the follow-up period. By multivariate analysis only the, hypertension, and presence of nephrotic range proteinuria during the follow-up period were the significant risk factors(14).

2. Hepatitis C virus (HCV)
People with the infection of hepatitis C virus (HCV) are at increased risk to develop glomerulonephritis(15).

3. Genetic passing through 
Primary glomerulonephritis with isolated C3 deposits: a new entity which shares common genetic risk factors with haemolytic uraemic syndrome(16)

4. Diabetes
There is a report of an 88-year-old man with a 30-year history of type 2 diabetes and a 3-year history of chronic renal failure was admitted for evaluation of anasarca. On admission, findings of nephrotic syndrome and microscopic hematuria were observed. During the course of therapy, rapid deterioration of renal function occurred with the appearance of pneumonia. Irrespective of the therapy with hemodialysis and antibiotics, he died of respiratory failure. The autopsy showed a rare case of rapidly progressive glomerulonephritis (crescentic glomerulonephritis) superimposed on membranous nephropathy(17)

4. Other risk factors
History of cancer, Blood or lymphatic system disorders, Exposure to hydrocarbon solvents are associated to higher risk to develop glomerulonephritis(17)

C. Complications 
1.  Heart failure (HF), acute renal failure (ARF), hypertensive encephalopathy and nephrotic range proteinuria
In the study of Systemic complications of acute glomerulonephritis in Nigerian children, by Dr. Olowu WA at the Obafemi Awolowo University Teaching Hospitals Complex, showed that majority of the patients (18/29) were under 6 years of age, with peak age incidence of 3 years. The hospital incidence of AGN and prevalence of systemic complications were 10 new cases per year and 41.38%, respectively. Heart failure (HF) and acute renal failure (ARF) were sole systemic complications in 7 and 2 AGN patients, respectively. Three patients had double systemic complications: one each of hypertensive encephalopathy (HTE)+HF, HTE+ARF and ARF+HF. Ten of 29 patients (34.48%) had nephrotic range proteinuria. None of the AGN patients except those with ARF had FeNa >1%, plasma bicarbonate <15 mmol/l, urea 225 mmol/l and creatinine 2400 mmol/l. Two of the patients died: one each of ARF and ARF+HF, giving a case fatality and mortality rate of 6.90% and 0.08%(18).


2. Chronic kidney failure
In most cases of glomerulonephritis (GN),  long-term course can lead to chronic renal failure(19).
 
3. Etc.

D. Diagnosis
After completing the physical exam and family history, the tests which your doctor orders include 
1. Urinalysis 
The aim of the test is to check
a. Damage to the glomeruli
If the test shows the presence of red blood cells and red cell in the urine.
b. Infection or inflammation
If the white blood cells are presented in the urine, in mmost case.
c.  Nephron damage
If the presence of protein is found in the urinary test.

2. Blood tests
The aim of the test is to check for the presence of wast products which will provide the information of kidney damage and impairment of the glomeruli

3. Imaging tests
Image test such as an ultrasound examination or a computerized tomography (CT) scan will provide visualization of the the damage of the patient kidneys.  

4. Kidney biopsy
The diagnosis of glomerulonephritis can be confirmed by performing a kidney biopsy. A small sample is extracted from the small pieces of kidney tissue for microscopic examination. The procedure is important in predicting the likely progress, response to treatment and outcome of  glomerulonephritis.

 In the analyzing whether histological diagnosis of glomerulonephritis (GN) at an early stage of chronic kidney disease (CKD) associated with different outcome and compared to diagnosis at a more advanced stage. Patients with CKD stage 1 and 2 at kidney biopsy had fewer endpoints compared to patients with a GFR of <60 ml/min (p < 0.001). Kidney function at the time point of histological glomerulonephritis (GN) diagnosis is associated with clinical outcome, likely due to early initiation of specific drug treatment. This suggests that selection of therapy yields greatest benefit before renal function is impaired in GN(20).

E. Prevention
E.1. The do`s and do not`s list
1. Diet to enhance your immune to prevent infection and inflammation caused by bacteria and virus, including HIV and hepatitis.

2.  Mediterranean diet
On the most healthy diet in the Southern Italy and Northern Greek. MeDiet score was created based on the intake of ten food components: vegetables; whole grains; nuts; legumes; fruits; ratio of monounsaturated:saturated fat; red and processed meat; dairy products; fish; alcohol. researchers at the University of Minnesota, in the study of Relationships of the Mediterranean dietary pattern with insulin resistance and diabetes incidence in the Multi-Ethnic Study of Atherosclerosis (MESA), showed that ahigher MeDiet score was also associated with significantly lower glucose levels after basic adjustment, but was attenuated after adjustment for waist circumference. During the follow-up, 412 incident diabetes events accrued. The MeDiet was not significantly related to the risk of incident diabetes (P for trend = 0·64). In summary, greater consistency with a Mediterranean-style diet, reflected by a higher a priori MeDiet score, was cross-sectionally associated with lower insulin levels among non-diabetics, and with lower blood glucose before adjustment for obesity, but not with a lower incidence of diabetes(21).

3. Stop smoking
Cigarette contains many harmful  chemicals, including cadmium. There is a significant association between blood cadmium levels and elevated blood pressure regardless of the type of variable (continuous or categorical) in women and men with a lower blood cadmium level compared to previous Korean studies, according to the study by the Soonchunhyang University(22),

4. Safe sex
Safe sex to prevent infection caused by sexual transmitting diseases.

5. Eat well to prevent fluctuation of insulin levels of that can increase the risk of diabetic nephropathy

6. Reduce intake of salt to prevent fluid retention, swelling and hypertension

7. Maintain healthy weight to prevent complications due to obesity

8. Etc.


E.2. Phytochemicals to prevent glomerulonephritis
1. (-)-epigallocatechin-3-gallate (EGCG)
In the study of Glomerulonephritis therapy: is there a role for green tea?, researchers at the Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, showed that (-)-epigallocatechin-3-gallate (EGCG) treatment ameliorates renal inflammation, tissue damage, and loss of renal function and might therefore represent a novel therapeutic approach for human glomerulonephritis(23).

2. Resveratrol
Mesangioproliferative glomerulonephritis is associated with overactive PDGF receptor signal transduction. We show that the phytoalexin resveratrol dose dependently inhibits PDGF-induced DNA synthesis in mesangial cells with an IC(50) of 10 microM without inducing apoptosis(24).

3. Isoflavones genistein and genistin 
In the study to evaluate the Male Wistar rats with glomerulonephritis caused by a single intravenous injection of nephrotoxic serum,with 5 mg of genistein or 8 mg of genistin/d/100 g body weight for 12 d given orrally, found that these isoflavones suppressed nephritis-induced severe hypercholesterolemia and hypertriglyceridemia, and their hypolipidemic action was almost identical. Fecal steroid excretion was unchanged by administration of the two isoflavones. Genistein inhibited the incorporation of [1-14C]acetate into cholesterol and FA in liver slices from nephritic rats when added to an incubation buffer, whereas genistin did not(25).

4. Etc.


E3. Diet to prevent Glomerulonephritis
1. Flaxseed
In the study to evaluate Flaxseed: a potential treatment for lupus nephritis, showed that 30 g flaxseed/day was well tolerated and conferred benefit in terms of renal function as well as inflammatory and atherogenic mechanisms important in the pathogenesis of lupus nephritis(26).

2. Green tea
In the study to investigate whether the anti-inflammatory and antioxidant properties of the green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) favorably affect the development of immune-mediated GN, researchers at the Shanghai Tenth People's Hospital of Tongji University, found that levels of glutathione peroxidase and peroxisome proliferator-activated receptor-γ (PPARγ), both reduced in the vehicle-pretreated diseased mice, were normalized. This renoprotective effect was reversed by concomitant administration of the PPARγ antagonist GW9662 throughout the EGCG pretreatment period. Importantly, mortality and renal dysfunction were significantly attenuated even when the polyphenol treatment was initiated 1 week after the onset of GN. Thus, EGCG reversed the progression of immune-mediated GN in mice by targeting redox and inflammatory pathways(27).

3. Soy
According to the study of Beneficial effects of soy protein consumption for renal function by Anderson JW. at the University of Kentucky, substituting soy protein for animal protein usually decreases hyperfiltration in diabetic subjects and may reduce urine albumin excretion. Limited data are available on effects of soy peptides, isoflavones, and other soy components on renal function on renal function in diabetes(28).


4. Etc.

F. Treatment 
F.1. In conventional medicine perspective
Treatment depends on the underlined causes, symptom and types of glomerulonephritis (Acute or chronic)
F.1.1. If the causes of the disease is the result of hypertension
Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. High blood pressure means raising pressure in your heart and staying high over time, damaging the body in many ways.
1. Diuretics
Thiazide diuretics were the first tolerated efficient antihypertensive drugs that significantly reduced cardiovascular morbidity and mortality in placebo-controlled clinical studies. Although these drugs today still are considered a fundamental therapeutic tool for the treatment of hypertensive patients. Thiazide diuretics must be used at appropriate and/or optimal doses to achieve the optimal antihypertensive effect with the smallest occurrence of side effects, including alterations in glucose and lipid profiles and hypokalemia. Moreover, because thiazide diuretics can increase the incidence of new-onset diabetes, especially when combined with beta blockers, caution is advised in using these drugs above all in patients who are at high risk for developing diabetes(29), according to the study by Department of Internal Medicine, University of Pisa(29).

2. Angiotensin-converting enzyme (ACE) inhibitors and Angiotensin II receptor agonists
In the study of a total of 25,035 hypertensive patients newly prescribed an ACE inhibitor or angiotensin II receptor blockers (ARBs), no differences were found in risk of death, coronary disease, chronic kidney disease, or stroke between those prescribed ACE inhibitors and those prescribed ARBs. Patients prescribed ARBs had a greater rate of new-onset diabetes (hazard ratio [HR], 1.28; confidence interval [CI], 1.08-1.52), and this was especially true for women (HR, 1.93; CI, 1.22-3.07). Within a large medical-practice based population, there was no evidence of differential effectiveness between ACE inhibitors and ARBs for most outcomes, with diabetes being the notable exception(30).

3. Etc.

A.2. If the causes of the disease is the result of infection due to invasion of bacteria
Corticosteroid therapy with antibiotics 

There is a report of a 24-years old man who presented to the hospital with fever, fatigue, and rapidly progressive glomerulonephritis. Although renal function in the case worsened despite therapy with antibiotics, a short-term and low dose of corticosteroid therapy with antibiotics was able to recover renal function and the patient finally underwent tricuspid valve-plasty and VSD closure, according to the study by Shiga University of Medical Science, Seta(31). 

A.3. Lupus or vasculitis
Lupus is a chronic, autoimmune disease as as a result of the development of autoantibodies that attack the systems and organs in the body.researchers at the indicated that saturated fatty acid palmitate, but not unsaturated oleate, induces the activation of the NLRP3-ASC inflammasome, causing caspase-1, IL-1β and IL-18 production. Immune-suppressing drugs can be prescribed to control inflammation. 
Immune-suppressing drugs
Tacrolimus, an immune-suppressing drug, at low dosage and serum level to be potentially effective and safe for treatment in patients with LN resistant to sufficient CYC therapy. A tacrolimus dosage of 2-3 mg daily appears to be effective and safe, according to the study by Peking Union Medical College Hospital, Chinese Academy of Medical Sciences(32)

A.4. IgA nephropathy
Treatment strategies have included management of blood pressure and lipids, improvement or stabilization of kidney function, and reduction of proteinuria. Supportive therapies, including angiotensin blockade, should be considered as first-line therapy for patients with urine protein >0.5 g/day and/or blood pressure >140/90 mm Hg. Corticosteroids could be considered as add-on or monotherapy for patients with urine protein >1 g/day with preserved renal function, but conclusive data are lacking for general treatment recommendations for the use of other therapies for IgAN(33).

A.5. Etc.
 B. In herbal medicine perspective
According to the research of Herbal treatments of glomerulonephritis and chronicrenal failure: Review and recommendations by Rainer Nowack, Felipe Flores-Suarez, Rainer Birck, Wilhelm Schmitt and Urs Benck(34), some herbs below may have certain effects in treating glomerulonephritis.
1. Astragalus
In the study to evaluate the effect of APS on glomerulonephritis rats induced by cationic Bovine Serum Albumin(C-BSA) by flow cytometry using Nuclear Transcription Factor-kappaB (NF-kappaB) as marker, showed that the expression of NF-kappaB and the concentration of IL-2, IL-6 and TNF-alpha were significantly decreased in the treatment group. This study clearly suggests that APS is effective in protecting against glomerulonephritis induced by C-BSA through the inhibition of NF-kappaB mediated-cytokine pathway(35).



2. Rhubarb
In the study of  the evidence of the effect of Rhubarb in immune complex GN induced in rats by injection of anti-thymocyte serum (ATS), researchers at the Department of Nephrology, Drum Tower Hospital, indicated that Rhubarb-treated anti-Thy-1 animal model should develop significantly less matrix expansion. Rhubarb also inhibited synthesis and secretion of fibronectin, an important component of mesangial extracellular matrix. Decreased IL-1 activity might be involved in the therapeutic effect of Rhubarb on mesangioproliferative glomerulonephritis(36).

3. Perilla frutescens
In the study to evaluate the anti-nephritic effects of perilla in HIGA mice that spontaneously develop high levels of serum immunoglobulin A (IgA) along with mesangial IgA deposition, researchers at the Graduate School of Pharmaceutical Sciences, Kyoto University, showed that Perilla suppressed proteinuria, proliferation of glomerular cells, serum levels of IgA, glomerular IgA and IgG depositions in HIGA mice. Cultured Peyer's patch cells and spleen cells from perilla-treated mice produced significantly less IgA than controls. Rosmarinic acid, by itself, suppressed serum IgA levels and glomerular IgA deposition in HIGA mice. Cultured spleen cells from RsA-treated mice produced less IgA than controls(37).


4. Dan Shen and Sheng Mai Ye
In the study to investigate the effects of danshen(Salvia plectranthoides Griff.) and shengmaiye (Panax ginseng C. A. Mey, Ophiopogon japonicus Ker-Gawl and Schisandra chinensis Baill) on glomerulosclerosis induced by adriamycin in SD rats, showed that Dansheng and shengmaiye may play an important role in the treatment of glomerulosclerosis in rats(38).

5. Arctium lappa
In the study of the ameliorative effects of arctiin from Arctium lappa on experimental glomerulonephritis in rats, researchers at the School of Pharmacy, Second Military Medical University, found that the ameliorative effects of arctiin on glomerulonephritis is carried out mainly by suppression of NF-kappaB activation and nuclear translocation and the decreases in the levels of these pro-inflammatory cytokines, while SOD is involved in the inhibitory pathway of NF-kappaB activation. Arctiin has favorable potency for the development of an inhibitory agent of NF-kappaB and further application to clinical treatment of glomerulonephritis, though clinical studies are required(39).

6. Etc. 


C. In Traditional Chinese medicine perspective 
 C.1. HTCM herbal formula: Huang Dan decoction (HDD) and Tripterygium Wilfordii (TW)
In the study to investigate the therapeutic effects of huangdan decoction (HDD) and Tripterygium Wilfordii (TW) compound tablet on membranous glomerulonephritis in rats, researchers at the Tongji Medical University, indicated that HDD and TW may alleviate the pathological lesions of MGN, prevent or retard its progression, and have remarkable therapeutic effects on MGN(40).

C.2. Shen Yan Yi Qi Ye 
In the study using cationic bovine serum albumin (C-BSA) for duplicating experimental animal model of membranous glomerulonephritis with chronic renal failure, found that in the therapeutic group, the urine protein and serum creatinine were reduced as compared with those in pathological group, P < 0.01. The parameter of morphometric analysis of glomeruli such as mean diameter, mean perimeter, mean surface area, mean volume, mean cross sectional area were all decreased, P < 0.01, the number of glomerular proliferative cells and thickness of glomerular capillary wall were all attenuated, P < 0.01, as compared with those in the pathological group. It suggested that SYYQY might alleviate the glomeruli lesions and benefit the renal functions, according to the study by Beijing University of TCM(41).

C.3. Etc,

Sources
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(2) http://www.ncbi.nlm.nih.gov/pubmed/7164407
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(4) http://www.ncbi.nlm.nih.gov/pubmed/20976140
(5) http://www.ncbi.nlm.nih.gov/pubmed/21437150
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(12) http://www.ncbi.nlm.nih.gov/pubmed/9590289 
(13) http://www.ncbi.nlm.nih.gov/pubmed/12091909
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II. Interstitial nephritis (Tubulo-interstitial nephritis) 
Interstitial nephritis is defined as a condition of inflammation of the spaces between renal tubules, affecting the interstitium of the kidneys and kidney function in wast removal.
A. Signs and symptoms 
In the study of Symptoms in patients with tubulo-interstitial nephritis, researchers at the School of Medicine, Juntendo University, indicated that in patients with acute TIN, marked
1. Fever,
2. Back or flank pain
3. CVA tenderness
4. Skin rash
5. Arthralgia
6. Cosinophilia and
7. Eosinouria are observed.
Clinical symptoms might be induced by glomerular, proximal tubular or distal tubular dysfunction in chronic TIN. Mild to moderate
8. Proteinuria
9. Edema
10. Hypertension
11. Azotemia
12. Glucosuria
13. Aminoaciduria
14. Polyuria and
15. Polydipsia are characteristic findings in patients with chronic TIN(1).


B. Causes and Risk factors
1. In the study of The outcome of acute interstitial nephritis: risk factors for the transition from acute to chronic interstitial nephritis, researchers at the Department of Nephrology, MHH, Hannover, Germany, in determination of risk factors for the development of chronic renal insufficiency, and thus, the transition from acute to chronic interstitial nephritis, showed that acute interstitial nephritis was found in 6.5% of all biopsies (64 patients with 68 episodes of acute interstitial nephritis); it was infection-induced in 10%, idiopathic in 4%, and drug-induced in 85% of the cases (antibiotics in 13 cases, analgesics in 17, non-steroidal anti-inflammatory drugs (NSAIDs) in 16, diuretics in 5, and various other drugs in 7). Renal insufficiency was reversible in 69% and permanent in 31% (12% partially reversible, 19% irreversible). The infection-induced and idiopathic types of acute interstitial nephritis were always reversible. Drug-related acute interstitial nephritis caused permanent renal insufficiency in 36% with a maximum of 56% in NSAID-induced cases. In drug-induced cases, intake of the suspected drug for more than a month prior to diagnosis caused permanent renal insufficiency in 88% and interstitial granuloma in 31%(2).

2. Impaired potassium and magnesium homeostasis and urinary losses are associated with the increased risk of acute tubulo-interstitial nephritis(3)

3. Hypercalcemia is a life-threatening disorder and is related primarily to neoplastic diseases and primary and secondary hyperparathyroidism and associated to the risk of Interstitial nephritis(4).

4. Allergic effect
A severe generalized multisystem allergic reaction occurred in a 16-month-old infant following the use of trimethoprim-sulfamethoxazole. Acute interstitial nephritis developed three weeks following the onset of this reaction and resolved after three months. This is the first description of this renal toxicity with TMP-SMX in a child(4a).

5. Etc.


C. Diseases associated with interstitial nephritis
1. Crohn's Disease
There is a report of s case of of granulomatous interstitial nephritis (GIN) associated with Crohn's disease (CD) was reported. GIN is a rare pathological finding in renal biopsy specimens. In a patient affected by CD, granulomas may be found in various tissues and organs such as lymph nodes, mesentery, liver, and lungs and occasionally in bones, joints, and skeletal muscle. Few cases of granuloma have been reported in the kidney, and it is not always possible to relate the presence of granuloma to CD, to other interstitial granulomatosis diseases, or to a drug-induced reaction(5).

2. Sjögren's syndrome
In the study of the tissue distribution of cellular adhesion molecules (ICAM-1, ELAM-1, VCAM-1) was studied in specimens from six normal human kidneys and in six biopsies from kidneys with tubulointerstitial nephritis associated with Sjögren's syndrome, researchers at the Toho University School of Medicine, showed that adhesion molecules were thought to play a role in the pathogenesis of tubulointerstitial nephritis and sialoadenitis associated with Sjögren's syndrome. It was thus concluded that the same inflammatory process that took place in the salivary glands to induce the characteristic tissue change of Sjögren's syndrome likely was operative in the renal tubulointerstitial tissue as well(6).

3. Uveitisa
There is a report of Clinical features and natural course of acute tubulointerstial nephritis and uveitis (TINU syndrome) in five adolescent patients (3 girls and 2 boys), according to Dr. Nikolić V, and reseach team(7)

4. Tuberculosis
Tuberculosis (TB) is a common disease worldwide, but kidney affection, i.e. tubulointerstitial nephritis (TIN) caused by Mycobacterium tuberculosis is rare. More frequent in patients with TB is drug induced TIN, i.e. the result of intensive antitubercular treatment(8). 

5. Castleman's disease
There is a report of a case of mesangial proliferative glomerulonephritis with interstitial nephritis associated with multicentric Castleman's disease (MCD) successfully treated with an anti-interleukin-6 receptor antibody (tocilizumab)(9).

6. Feline morbillivirus
Feline morbillivirus, a previously undescribed paramyxovirus associated with tubulointerstitial nephritis in domestic cats(10)



7.  Etc.   

D. Diagnosis
Dr. Nikolić V and the research team in the review of the data between 1986 and 1997 of 21 patients, aged 7-16 years (mean, 12.8), with acute tubulointerstitial nephritis, including eight with tubulointerstitial nephritis and uveitis (TINU syndrome). Laboratory studies included urinalysis, complete blood count, erytrocyte sedimentation rate (ESR), plasma creatinine, glomerular filtration rate (GFR), electrolytes, proteins, IgG, C3, C4 antinuclear-antibodies (ANA), antistreptolysin-O and antibodies to hantaviruses. Renal ultrasound was done in all patients. Renal biopsy was performed in 5 children(11).


E. Prevention
1. Avoid overdose of medication and vitamins
Overdose of certain medication indicated above and some vitamins are associated to the increased risk of the diseases.
2. Eat well to enhance the immune system to prevent bacterial and viral causes of inflammation.
3. Use herbs with caution
Overdose of herb can damage to kidney of that can lead to interstitial nephritis(11a).
4. Avoid extreme Exercise
There is a report of a A 45-year-old man presented with abdominal pain, vomiting, and oliguria after severe exercise as a result of Familial renal hypouricemia with exercise-induced acute renal failure (ARF)(12).
5. Reduce in take of animal fat to prevent waste to the kidney
6. Reduce intake of salt to reduce the risk of hypertension and kidney overload.
7. Etc.
 
F. Treatment 
F.1. In conventional medicine perspective
1. Acute tubulointerstitial nephritis
In the study to evaluate the controversial effects of steroids in acute tubulointerstitial nephritis (ATIN), showed that steroid treated (StG) patients had a greater degree of improvement in their renal function; however there was no correlation between the degree of improvement in eGFR and delay in starting steroids. PPIs were second commonest implicated drug category among drug induced cases(13).

2. Chronic tubulointerstitial nephritis
Chronic tubulointerstitial nephritis has no cure. Many patients may require dialysis. In younger patient,  kidney transplant may be the only choice. 

F.2. In herbal medicine perspective
1. Soy
In the study to evaluate the effects of soy protein isolate (SPI) on severe kidney damage in deoxycorticosterone acetate (DOCA) salt-treated obese Zucker rats, researchers at the Food Science Research Institute, Fuji Oil Company Ltd., Izumisano-shi, showed that that consecutive treatment of SPI protects against renal dysfunction, particularly tubulointerstitial nephritis, in DOCA salt-treated obese Zucker rats(14).

2.  Flaxseed
In the study to determine if flaxseed would also modify clinical course and renal pathology in the Han:SPRD-cy rat, showed that Flaxseed ameliorates Han:SPRD-cy rat polycystic kidney disease through moderation of the associated chronic interstitial nephritis. The diet alters renal content of polyunsaturated fatty acids in a manner that may promote the formation of less inflammatory classes of renal prostanoids(15).

3. Etc.
 
F.3. In traditional Chinese medicine perspective 
1. Traditional Chinese medicine with immunosuppressant
In an  experimental study combined on traditional Chinese medicine with immunosuppressant for treatment and prevention of tubular interstitial nephritism researchers at the Department of Nephrology, First Affiliated Hospital, showed that the infiltration of cells was inhibited in the "Chinese herbs combined with prednisone" group, the infiltration of cells, TGF-beta expression and interstitial fibrosis were all inhibited in the cyclophosphamide and prednisone" group. But in the prednisone group, interstitial fibrosis was not inhibited. These data suggest that the combined use of Chinese herbs, immunosuppressant and prednisone can inhibit the interstitial cell infiltration and prevent the interstitial fibrosis in diffuse proliferative glomerulonephritis(16).

2. Astragali Radix and Angelicae Sinensis Radix (AS-IV)with ferulic acid
Other researchers suggested that AS-IV synergizes with FA to alleviate renal tubulointerstitial fibrosis; this was associated with inhibition of tubular epithelial-mesenchymal transdifferentiation (EMT) and fibroblast activation, as well as an increase in NO production in the kidney(17).
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/7563629
(2) http://www.ncbi.nlm.nih.gov/pubmed/11020015
(3) http://www.ncbi.nlm.nih.gov/pubmed/4058627
(4) http://www.ncbi.nlm.nih.gov/pubmed/19356379 
(4a) http://www.ncbi.nlm.nih.gov/pubmed/7149348
(5) http://www.ncbi.nlm.nih.gov/pubmed/22871108
(6) http://www.ncbi.nlm.nih.gov/pubmed/9524776
(7) http://www.ncbi.nlm.nih.gov/pubmed/17974468 
(8) http://www.ncbi.nlm.nih.gov/pubmed/22704252 
(9) http://www.ncbi.nlm.nih.gov/pubmed/22687845 
(10) http://www.ncbi.nlm.nih.gov/pubmed/22431644 
(11)  http://www.ncbi.nlm.nih.gov/pubmed/15637986
(11a) http://www.ncbi.nlm.nih.gov/pubmed/10676733
(12) http://www.ncbi.nlm.nih.gov/pubmed/14655203
(13) http://www.ncbi.nlm.nih.gov/pubmed/22817666
(14) http://www.ncbi.nlm.nih.gov/pubmed/22553937 
(15) http://www.ncbi.nlm.nih.gov/pubmed/9987066
(16) http://www.ncbi.nlm.nih.gov/pubmed/12515139 
(17) http://www.ncbi.nlm.nih.gov/pubmed/21232035

Ascariasis

Ascariasis is defined as a condition caused by round worm, the parasite Ascaris lumbricoides as a result of eating contaminated foods and  the human feces with Ascaris eggs. The disease infects over billions people around the globe, mostly in the third world.

I. Signs and symptoms
1. Intestinal obstruction 
In the study to describe the occurrence and management of bowel obstruction caused by Ascaris lumbricoides, a common parasite in warm climates that affects children with limited socioeconomic means, researchers at the Universidad Nacional de Colombia, Hospital de La Misericordia, showed that
physicians should have a high index of suspicion for parasitic infestation in warm climates where economically deprived children present with symptoms of intestinal obstruction. Ascaris lumbricoides may be the cause of these events in endemic areas(1).

2. Persistent cough, shortness of breath, wheezing
The affects of  hatching eggs of the round worm travel from the intestine  through the bloodstream or lymphatic system to the lungs where they are coughed up and swallowed can cause the symptoms of persistent cough, shortness of breath, wheezing, etc.

3. The adult round worm in the intestine where they grow and die can cause the symptoms of
a. abdominal pain, tenderness and bloating
Ascariasis is the most common helminthic infection in developing countries. It may cause chronic abdominal pain, tenderness and bloating(2). 

b. Nausea and vomiting
The symptoms are caused by toxin released by the round worm.

c. Bloody stools
It is a ewsult of inflammation caused by large numbers of Ascaris lumbricoides

4. Bowel obstruction
Bowel obstruction  can be caused by a large number of worms and various toxins released by the worms(3).

5. The presence of large numbers of round worm can cause symptoms
Severe abdominal pain, fatigue, vomiting, weight loss as the result of toxin released by large numbers of the adult worms and malnutrition.

6. In children
The presence of large numbers of roun woem can cause symptoms of the pain in periumbilical area, abdominal distension, interloop fluid, free fluid in the pelvis, etc(4).

7.  Malnutrition
There is a report of a case of a child three years old, with severe malnutrition as complication of Ascaris lumbricoides infection. Intestinal nematodes infect many of the world's children and constitute a formidable public health problem. The infected children may suffer nutritional deficits, serious illness and occasionally death(5).

8. Etc.

II. Causes and Risk factors
A. Causes
Ascariasis is a result of eating contaminated foods and  the human feces with Ascaris eggs.

B. Risk factors 
1. Children with male gender
Boys who live in the third world are the increased risk to develop Ascariasis. In the prospective study of 360 patients, researchers found that the male to female ratio was 1.37:1. 187 patients (52%) presented within 2-4 days of duration of illness. Mean +/- standard deviation (SD) age of patients was 6.35 +/- 2.25 years. Age group of 4-7 years (80%) was commonest group affected(6).


2. Trauma and tropical disease
There is a report of  a case of heavy intestinal infestation with Ascaris lumbricoides complicating the surgical management of a gunshot injury to the abdomen. Co-existent traumatic and infectious pathologies in this case highlight the complex burden of illness among children living in areas of violent conflict, with clinical relevance to trauma surgeons in the tropics(7).

3. Household cluster
Analysis of such data established that individuals are predisposed to infection with few or many worms and members of the same household tend to harbor similar numbers of worms. These effects, known respectively as individual predisposition and household clustering, are considered characteristic of the epidemiology of ascariasis. The mechanisms behind these phenomena, however, remain unclear, according to Dr. Walker M and the research team at the School of Public Health, Imperial College London(8). 

4. Poor sanitation
Use of human feces as fertilizer in the under developing world can increase the risk of  Ascariasis.

5. Etc.

III. Complications and diseases associated with Ascariasis
1. Pancreatitis
There is a report of  a 59-year-old female patient who was admitted for acute abdominal pain, having had several previous similar events before one of them was diagnosed as acute idiopathic pancreatitis. On admission, her physical exam was normal. Laboratory results showed hemoglobin 12.2 g/dL, white blood cell count 11 900 cells/mm(3), eosinophils 420 cells/mm(3), serum amylase 84 IU/mL, lipase 22 IU/mL and normal liver function tests. Abdominal ultrasound and a plain abdominal X-ray were also normal. An upper endoscopy showed round white worms in the duodenum and the stomach, some of them with bile in their intestines. The intestinal parasites were diagnosed as Ascaris lumbricoides(9)

 2. Esophageal space-occupying lesion
There is a report of an old female presented with dysphagia after an intake of several red bean buns and haw jellies. The barium meal examination revealed a spherical defect in the lower esophagus. Upper gastrointestinal endoscopy was done to further confirm the diagnosis and found a live Ascaris lumbricoides in the gastric antrum and two in the duodenal bulb(10).

3. Others
Ascaris infection is acquired by the ingestion of the embryonated eggs. The larvae, while passing through the pulmonary migration phase for maturation, cause ascaris pneumonia. Intestinal ascaris is usually detected as an incidental finding. Ascaris-induced intestinal obstruction is a frequent complication in children with heavy worm loads. It can be complicated by intussusception, perforation, and gangrene of the bowel. Acute appendicitis and appendicular perforation can occur as a result of worms entering the appendix. HPA is a frequent cause of biliary and pancreatic disease in endemic areas. It occurs in adult women and can cause biliary colic, acute cholecystitis, acute cholangitis, acute pancreatitis, and hepatic abscess. RPC causing hepatic duct calculi is possibly an aftermath of recurrent biliary invasion in such areas, according to the study by Dr. Khuroo MS. at the Sher-i-Kashmir Institute of Medical Sciences, Soura, Srinagar(11).

4. Etc.

IV. Diagnosis
After completing the physical examination and family history is recorded, the tests which your doctor order, include
1. Stool test
The aim of the test is to diagnose the presence of worm and egg in the stool.

2. Blood test 
The aim of the blood test is to diagnose for the presence of Eosinophil granulocyte, the white blood cells are  responsible for combating multicellular parasites and certain infections. There is a report of a  case of Ascaris-induced eosinophilic pneumonitis in an HIV-infected patient is described. Owing to his HIV status and the absence of peripheral blood eosinophilia on admission, the initial diagnosis was incorrect until the passage of two worms in his stool(12).

3. Abdominal X-rays
Abdominal X-rays is to test for the presence of the worm in the abdomen.

4. Ultrasound
the aim of the ultrasound is to check for the presence of worm in the internal organs. 

5. CT scans or MRI
The CT scan and MRI is to allow the doctor to examine the internal organs and their surrounding area, such as blocking ducts in your liver or pancreas to test for the presence of worms.

6. Etc.

 V. Prevention
If you are traveling to the rural in the third world
1. Wash you hands with soap before handing foods
2. Avoid using public washroom if you can
3. Cook you foods and water before consuming
4. Other researchers suggested that With the 3-year's intervention, the Ascaris lumbricoides infection rates decreased from 17.81% to 2.52%, the rate of mass chemotherapy was 81.65%, which covered more than 6.2 million person-time, the awareness rates of parasitic disease control knowledge among the residents raised from 45.11% to 95.99%, and 84.09% of local people were supplied with safe water and 50.30% of families had sanitary toilets(13).
According to the World Health Organization,  preschool and school-age children, women of childbearing age (including pregnant women in the 2nd and 3rd trimesters and lactating women) and adults are at the high risk of heavy infections.

VI. Treatment
A. Medication
The primary medication used to treat Ascariasis, including the recommendation of WHO by killing the worm with side effects of diarrhea and abdominal pain
Researchers at the Instituto de Biomedicina. Facultad de Medicina, UCV., showed that in addition to the WHO recommended drugs (albendazole, mebendazole, levamisole, and pyrantel pamoate), new anthelmintic alternatives such as tribendimidine and Nitazoxanide have proved to be safe and effective against A. lumbricoides and other soil-transmitted helminthiases in human trials. Also, some new drugs for veterinary use, monepantel and cyclooctadepsipeptides (e.g., PF1022A), will probably expand future drug spectrum for human treatments(14).


B. Surgery
The aim of the surgery is to repair the damage caused by the worm and treatment of the medication, such as  Intestinal obstruction, bile duct obstruction, bleeding, thromboembolism, perforation, etc(15)(16).
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For over 100 healthy recipes, http://diseases-researches.blogspot.ca/p/blog-page_17.html

Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/8632280
(2) http://www.ncbi.nlm.nih.gov/pubmed/20447214
(3) http://www.ncbi.nlm.nih.gov/pubmed/22262337 
(4) http://www.ncbi.nlm.nih.gov/pubmed/20143068
(5) http://www.ncbi.nlm.nih.gov/pubmed/9173412
(6) http://www.ncbi.nlm.nih.gov/pubmed/20143068
(7) http://www.ncbi.nlm.nih.gov/pubmed/20431222
(8) http://www.ncbi.nlm.nih.gov/pubmed/21541362
(9) http://www.ncbi.nlm.nih.gov/pubmed/20447214
(10) http://www.ncbi.nlm.nih.gov/pubmed/22509089
(11) http://www.ncbi.nlm.nih.gov/pubmed/8863040
(12) http://www.ncbi.nlm.nih.gov/pubmed/17264245
(13) http://www.ncbi.nlm.nih.gov/pubmed/22263492
(14) http://www.ncbi.nlm.nih.gov/pubmed/20701574
(15) http://www.ncbi.nlm.nih.gov/pubmed/20037884
(16) http://www.ncbi.nlm.nih.gov/pubmed/21698086

Thursday, October 25, 2012

Gallstone

A gallstone formed within the gallbladder as a result of changes in bile acid (BA) metabolism and gallbladder function are critical factors in the pathogenesis of gallstones. Gallstones can cause blockage the flow of bile through the bile ducts that can lead to inflammatory causes of  acute cholecystitis. Gallstones are most common among older adults, women, overweight people, etc.
 

A. Symptoms  
A.1. Common symptoms

1. Upper gastrointestinal bleeding if ruptured
There is a report of a 67-year-old gentleman with no significant medical history of note presented with sudden onset of epigastric pain, coffee ground vomiting and passing black tarry stool. The diagnosis of gallstone-induced auto-sphincterotomy was only made, using gastroscope via jejunostomy, when a big gallstone was found in the third part of the duodenum and the papilla was ruptured(1).

2. Right upper quadrant or midline epigastric pain
In a  multicenter study was carried out with patients randomized to either surgery or conservative, expectant treatment to examine optimal treatment and natural history in well-defined groups of symptomatic gallbladder stone disease with pain, episodes only (study group 1) or acute cholecystitis (study group 2). The patients were between 18 and 80 years of age and had right upper quadrant or midline epigastric pain and ultrasonographic evidence of gallbladder stone, with or without acute cholecystitis(2).

3. Abdominal pain
Gallstones are relatively rare in children. At-risk populations include patients suffering from hemolysis syndromes. Regardless of etiology, these patients usually will present with postprandial abdominal pain, and ultrasonography is the mainstay of diagnosis. However, some gallstones are radiopaque and can be visualized on plain abdominal radiography(3).

4. Other symptoms
In the study to evaluated the association between gallstones and abdominal symptoms, comparing two different study designs, researchers at the Maastricht University, showed that Gallstones were associated with mid upper abdominal pain in the screening study, and with mid upper abdominal pain, biliary pain, and colic (each independently) in the clinical study. When these symptoms were absent (and only dyspeptic symptoms or food intolerance was present), gallstones were not more common than expected from the general population prevalence (estimated from the screening study)(4).

5. Etc. 

A.2. Symptoms of severe case, include
1. Fever
2. Nausea and vomiting
3. Prolonged period of pain
4. Jaundice
5. Clay-colored stools
6. Etc.

 

B. Causes and Risk factors
B.1. Causes
 High cholesterol or bilirubin in the bile 
Gallstones are precipitations of oversaturated bile fluid. They can develop in the gallbladder and in the efferent bile ducts; they are very often correlated with diseases of the gallbladder, bile ducts and neighboring organs(5).

B.2. Risk factors
1. hypertriglyceridemia, overweight and insulin resistant
 Patients with hypertriglyceridemia (HTG) - often overweight and insulin resistant - are at risk for gallstone disease(6).

2. Pregnancy and gender
Pregnant women(6b)  and Elder are at higher risk to develop (specially, pigment stones in elder) gallstones(6a)

3. Haemoglobin E beta thalassaemia
in the study to  determine whether this has a genetic basis we compared the bilirubin levels and frequency of gallstones in patients with different alleles of the UGT*1 gene, showed that the UGT*1 genotpe is of importance in the genesis of gallstones in this population of patients(7).


4. Obesity and weight loss
In the study to investigate the relation of obesity and weight loss to the formation of gallstones according to pertinent clinical and research issues, showed that during weight loss, particularly among the obese, an increased risk exists for symptomatic gallstone formation. This acute risk offers the opportunity to investigate the cause of gallstones and possibly to prevent them(8).

5. Diet
Diet with high in saturated fat  and low in fiber increase the risk of gallstones as a result of  increased cholesterol in the bile.

6. Ethnicity
Certain races may be at the increased of the development of gallstone such as American Indians, Mexican  have a genetic predisposition to secrete high levels of cholesterol in bile.

7. Hormone replacement therapy in postmenopausal women and oral contraceptives have also been described to be associated with an increased risk for gallstone disease(8a).

C. Diagnosis
After completing the physical examination and family history, if gallstones are suspected, the tests which your doctor orders include
1. Blood tests
The aim of the blood test is to look for the signs of infection, obstruction, pancreatitis, jaundice, liver enzymes, etc.

2. Ultrasonography 
The aim of the test is to look for the images of the abnormalltyof gallbladder and its surrounding area, including the thickened wall of the gallbladder when there is cholecystitis, pancreatitis, enlarged gallbladder, bile duct obstruction, etc.

3. Computerized tomography (CT) scan
the aim of the CT scan to allow your doctor to visualize the gallbladder and its surrounding area, including gallstones, infection, rupture of gallbladder, etc..

4. Cholescintigraphy (HIDA scan)
The aim of the test is to diagnose the abnormal contraction of the gallbladder with the injection of with a small amount of radioactive material


5. Endoscopic retrograde cholangiopancreatography (ERCP)
With the local anesthesia and the use of a The endoscope, your doctor can visualize the gallstone and remove them if found. 

6. Etc.

D. Complications and Diseases associated with gallstone 
1. Spontaneous cholecystocutaneous fistula
Spontaneous perforation of gallbladder as a complication of biliary stones may lead to a cholecystocutaneous abscess or fistula. The pathophysiology of this condition has been associated with increased pressure in the gallbladder, secondary to biliary obstruction(9).

2. Jaundice
In the study to evaluate 56 patients with obstructive jaundice, the presence or absence of calculi in the gallbladder has been correlated with the cause of the obstruction. Seven of 23 patients with obstruction caused by stone had no calculi in the gallbladder. Twelve of 33 patients with obstruction due to tumor also had gallstones. It was concluded that the presence of calculi in the gallbladder is a poor indicator of the cause of obstructive jaundice(10).

3. Others diseases associated with gallstones
a. In Children
In the review of the risk factors, complications, and outcomes of gallstones at our institution, particularly in those patients who are asymptomatic at the time of initial diagnosis, researchers at the The Hospital for Sick Children, Toronto, showed that at diagnosis, 50.5% of children were asymptomatic; these patients were diagnosed at a mean age of 8.23 years. Compared with symptomatic patients, they were less likely to have a hemolytic anemia but more likely to have other risk factors, including cardiac surgery, leukemia and lymphoma, short bowel syndrome, or exposure to total parenteral nutrition or cephalosporins(11). 

b. In Adult
Gallstones cause various problems besides simple biliary colic and choplecystitis. With chronicity of inflammation caused by gallstone obstruction of the cystic duct, the gallbladder may fuse to the extrahepatic biliary tree, causing Mirizzi syndrome, or fistulize into the intestinal tract, causing so-called gallstone ileus. Stones may pass out of the gallbladder and travel downstream through the common bile duct to obstruct the ampulla of Vater resulting in gallstone pancreatitis, or pass out of the gallbladder inadvertently during surgery, resulting in the syndromes associated with lost gallstones(12).

E. Prevention
1. Vegetable
Vegetable protein may reduce the risk of cholelithiasis(19)

2. A low-fat, low-protein, high-carbohydrate or lowering of glycaemic index and the caloric reduction diet may reduce the risk of formation of gallstone formation(21)

3. Reduce intake of bad fat(23)
In the study of found  that  the type of dietary fat habitually consumed can influence bile composition in humans. In gallbladder, this influence was noted in the presence of more concentrated bile in the olive oil group. However, this was not translated into a modification of cholesterol saturation, which is likely due to the fact that cholesterol gallstones were present by the time the dietary intervention started(22).

4. Nuts
Nuts (tree nuts and peanuts) are nutrient dense foods with complex matrices rich in unsaturated fatty and other bioactive compounds: high-quality vegetable protein, fiber, minerals, tocopherols, phytosterols, and phenolic compounds According to the study by Dr, Ros E nuts are likely to beneficially impact health outcomes. Epidemiologic studies have associated nut consumption with a reduced incidence of coronary heart disease and gallstones in both genders and diabetes in women(20).

5. Wheat bran
There is a study of 10 patients with probable cholesterol gallstones took bran supplements for 4-6 weeks, their gallbladder bile aspirated from the duodenum became less saturated with cholesterol(24).

6. Others
Some researchers suggested that intake of high energy, simple sugar and saturated fat favors gallstone formation. Fiber and moderate consumption of alcohol reduce the risk(25).



F. Treatment
F.1. In conventional medicine perspective
1. Cholecystectomy
No treatment for people who have developed galldtones but with no system, otherwise, surgery to remove the gallbladder may be necessary. Cholecystectomy is the surgical removal of the symptomatic gallbladder. In the sugery, It is the most common method for treating symptomatic gallstones, other surgeries include the  laparoscopic cholecystectomy, and an older more invasive procedure, called open cholecystectomy.

2. Others
a. Some researchers suggested for the treatment of gallstones in patients with normal stonefree bile ducts, new modalities have been developed besides the classical cholecystectomy and the oral litholysis. The interventional procedures (local litholysis, extracorporeal shockwave lithotripsy, combination of shockwave lithotripsy and local litholysis, cholecystostomy and extra- or intracorporeal lithotripsy) do not need a narcosis and can be applied even in high-risk patients. Because the gallbladder itself is not removed, the recurrence rate after all these interventions is rather high. The new operative procedures (laparoscopic cholecystectomy, mini-laparotomy cholecystectomy) are definitive solutions for stone disease, but must be performed mostly in narcosis(13).

b. Today, cholecystectomy was still the most frequent method of treatment for symptomatic cholecystolithiasis (n = 1369) with low morbidity (4.3%) and lethality (0.28%). Probably less than 20% of all cases fulfill the strict selection criteria for extracorporeal shock wave lithotripsy (ESWL). All alternative methods of treatment in which the gallbladder is preserved have an increased risk for gall stone recurrence. Only after the long-term follow-up results of ESWL are known, the recurrence rate can be assessed. In most cases, bile duct stones (n = 417) were removed by endoscopy, if necessary in combination with ESWL (n = 310, stone removal: 95%, lethality: 0.3%). However, in low risk patients with concurrent cholecystolithiasis surgery was still the method of choice (n = 107, stone removal: 96%, lethality: 0/107)(14).

F.2. In herbal medicine perspective
1. Fenugreek seeds and onion
In the study to evaluate the antilithogenic effect of a combination of dietary fenugreek seeds and onion, researchers at the Central Food Technological Research Institute, found that hepatic lipid peroxides were reduced by 19-22% and 39-45% with fenugreek, onion and their combination included in the diet along with the HCD. Increased accumulation of fat in the liver and inflammation of the gallbladder membrane produced by HCD were reduced by fenugreek, onion and their combination. The antilithogenic influence was highest with fenugreek alone, and the presence of onion along with it did not further increase this effect(15).

2. Capsaicin and curcumin
In the study of the efficacy of capsaicin and curcumin in cholesterol gallstones induced by feeding mice a high-cholesterol (0.5%) diet for 10 weeks, found that the capsaicin and curcumin combination did not have an additive influence in reducing the incidence of cholesterol gallstones in mice, their combination nevertheless was more beneficial in enhancing the activity of hepatic antioxidant enzyme ─ glutathione reductase in the lithogenic situation. The antioxidant effects of dietary spice compounds are consistent with the observed reduction in cholesterol gallstones formed under lithogenic condition(16).

3. Garlic and onion
The Central Food Technological Research Institute has reported the study of the health beneficial potential of dietary garlic and onion in reducing the incidence and severity of cholesterol gallstone (CGS)with the induced CGS in mice with a lithogenic diet for 10 weeks, they were maintained on basal diets containing 0.6% dehydrated garlic or 2% dehydrated onion for a further 10 weeks(26). Others suggested that dietary allium spices exerted antilithogenic influence by decreasing the cholesterol hyper-secretion into bile and increasing the bile acid output thus decreasing the formation of lithogenic bile in experimental mice(27).

4. Milk thistle
There is a study indicated that after intake of milk thistle bile duct hyperplasia were significantly decreased in 50,000 ppm males and in all exposed groups of females, and the incidence of mixed inflammatory cell infiltration was significantly decreased in 50,000 ppm males(28).


5. Etc.

F.3. In traditional Chinese perpective
1. Traditional Chinese herbs for nourishing the liver (Yanggan Lidan Granule (YGLDG))
In the study of Eighty guinea pigs randomly divided into four groups, which were normal control group, untreated group, nourishing-liver Chinese drug (NLCD) group and ursodeoxycholic acid (UDCA) group, with 20 guinea pigs in each group, gallstones were induced in the guinea pigs of the latter 3 groups by the feed of diet inducing cholelithiasis with high cholesterol, while the corresponding medicines were used in NLCD group and UDCA group for prevention and treatment for 7 weeks, showed that the [Ca(2+)]i in gallbladder cells is the important factor for contractile function of gallbladder and the information of gallstones. Traditional Chinese herbs for nourishing the liver may significantly increase the [Ca(2+)]i in gallbladder cells to facilitate contraction of the smooth muscle cells of gallbladder and relieve the cholestatis(17).
Other study to explore the effects of Yanggan Lidan Granule (YGLDG), a compound traditional Chinese herbal medicine for nourishing liver and improving choleresis, on the rate of gallstone formation and content of plasma cholecystokinin in guinea pigs with induced cholesterol gallstones. indicated that YGLDG can significantly decrease the rate of gallstone formation in guinea pigs. It may be related to elevating the content of CCK in the plasma(18).

2. Ingredients of Yanggan Lidan Granule (YGLDG) 
a. Bai Shao tonifies liver Yin,
b. Chen Pi,
c. Gao Qi Zi tonifies liver Yin
d. He shou wu tonifies liver Yin
e. Gan Cao
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/22914239
(2) http://www.ncbi.nlm.nih.gov/pubmed/9200296
(3) http://www.ncbi.nlm.nih.gov/pubmed/22888958
(4) http://www.ncbi.nlm.nih.gov/pubmed/9802450
(5) http://www.ncbi.nlm.nih.gov/pubmed/423995
(6) http://www.ncbi.nlm.nih.gov/pubmed/20699090
(6a) http://www.ncbi.nlm.nih.gov/pubmed/7771432
(6b) http://www.ncbi.nlm.nih.gov/pubmed/17103289
(7) http://www.ncbi.nlm.nih.gov/pubmed/11425418
(8) http://www.ncbi.nlm.nih.gov/pubmed/8214980
(8a) http://www.ncbi.nlm.nih.gov/pubmed/17103289
(9) http://www.ncbi.nlm.nih.gov/pubmed/22794521
(10) http://www.ncbi.nlm.nih.gov/pubmed/7434173
(11) http://www.ncbi.nlm.nih.gov/pubmed/20118803
(12) http://www.ncbi.nlm.nih.gov/pubmed/18992599 
(13) http://www.ncbi.nlm.nih.gov/pubmed/2028140
(14) http://www.ncbi.nlm.nih.gov/pubmed/2721300
(15) http://www.ncbi.nlm.nih.gov/pubmed/21756271
(16) http://www.ncbi.nlm.nih.gov/pubmed/21609281
(17) http://www.ncbi.nlm.nih.gov/pubmed/17352876
(18) http://www.ncbi.nlm.nih.gov/pubmed/18405610 
(19) http://www.ncbi.nlm.nih.gov/pubmed/1503808
(20) http://www.ncbi.nlm.nih.gov/pubmed/22254047
(21) http://www.ncbi.nlm.nih.gov/pubmed/14619611
(22) http://www.ncbi.nlm.nih.gov/pubmed/15797676
(23) http://www.ncbi.nlm.nih.gov/pubmed/1398503
(24) http://www.ncbi.nlm.nih.gov/pubmed/941893
(25) http://www.ncbi.nlm.nih.gov/pubmed/15190042
(26) http://www.ncbi.nlm.nih.gov/pubmed/20153000
(27) http://www.ncbi.nlm.nih.gov/pubmed/18983715
(28) http://www.ncbi.nlm.nih.gov/pubmed?term=Milk%20thistle%20and%20gallstone

Friday, October 19, 2012

Kidney stones (Renal calculus)

Kidney stones is a composed of mineral salts formed in the kidneys. Men account for the 80% of those with kidney stones and are at risk of the formings between 30 and 40 years of age. About 75% of kidney stones are calcium stones.

I. Symptoms
Some people with kidney stones may not experience any symptom at all. Renal colic is characterized by an excruciating intermittent pain, usually in the flank (the area between the ribs and hip), that spreads across the abdomen, often to the genital area and inner thigh. The pain tends to come in waves, gradually increasing to a peak intensity, then fading, over about 20 to 60 minutes. The pain may radiate down the abdomen toward the groin or testis or vulva.

Other symptoms include nausea and vomiting, restlessness, sweating, and blood in the urine. A person may have an urge to urinate frequently, particularly as a stone passes down the ureter. Chills, fever, and abdominal distention sometimes occur.(1a)

II. Causes and Risk factors
A. Causes
1. Dehydration 
Dehydration or strenuous exercise without adequate fluid can cause the forming of kidney stones as a result of low levels of urine pH (below 5.5)(1).

2. Ramadan fasting ( food restriction)
Ramadan fasting are associated with risk of kidney stones forming. In the study to evaluate the effects of fluid and food restriction in Ramadan fasting on urinary factors in kidney and urinary calculus formation, researchers at the Shahid Beheshti University of Medical Sciences, found that fasting during Ramadan has different effects on total excretion and concentrations of urinary precipitate and inhibitory factors contributing to calculus formation(2).

3. Rotavirus infection
There is a report of  4 patients with RV infection who developed postrenal renal failure induced by urinary tract obstruction with uroammoniac calculi or crystals... Uric acid stone formation was considered to have originated from the low pH caused by dehydration and the increase of urinary uric acid excretion from damaged cells(3).

4. Calcium
In the study to explore the relationship among intestinal fractional calcium absorption, calcium intake and nephrolithiasis in a prospective cohort of 9,704 postmenopausal women recruited from population based listings in 1986 and followed for more than 20 years, showed that fractional calcium absorption is higher in women with a history of nephrolithiasis. Higher intestinal fractional calcium absorption is associated with a greater risk of historical nephrolithiasis. Dietary and supplemental calcium decrease fractional calcium absorption, and may protect against nephrolithiasis(3a).

5. Gastrointestinal lipase inhibitor
Intestinal malabsorption can cause urinary stone disease via enteric hyperoxaluria. The use of lipase inhibitors, especially under a diet rich in oxalate alone or associated with fat, leads to a significant and marked increase in urinary oxalate and a slight reduction in uCa and uMg that, taken together, resulted in an increase in AP (CaOx) index(rat), elevating the risk of stone formation(3b).

6. High fat intake
A comparison of the dietary intake per kilogram body weight in each group was made using standard statistical procedures. None of the nutrient intakes showed a significant difference, but dietary fibre intake and the percentage of energy provided by carbohydrate were consistently higher in the control group, whereas the percentage of energy provided by fat was consistently higher in the renal stone group(3c).

7. Vitamins
In the study of a total of 1078 incident cases of kidney stones was documented during the 14-yr follow-up period. A high intake of vitamin B6 was inversely associated with risk of stone formation. After adjusting for other dietary factors, the relative risk of incident stone formation for women in the highest category of B6 intake (> or =40 mg/d) compared with the lowest category (<3 mg/d) was 0.66 (95% confidence interval, 0.44 to 0.98). In contrast, vitamin C intake was not associated with risk. The multivariate relative risk for women in the highest category of vitamin C intake (> or =1500 mg/d) compared with the lowest category (<250 mg/d) was 1.06 (95% confidence interval, 0.69 to 1.64). Large doses of vitamin B6 may reduce the risk of kidney stone formation in women. Routine restriction of vitamin C to prevent stone formation appears unwarranted(3d).

8. Etc.

B. Risk factors
1. Gender
If you are men, you are at higher risk to develop kidney stones. In the study to determine gender differences in the symptomatic presentation of kidney and ureteral stones among the Hispanic population and compared it with presentation in the Caucasian population, found that the male-to-female ratio of the symptomatic patients with kidney stones was 1.48 for both Hispanic and Caucasian patients. The male-to-female ratio for ureteral stones was 1.06 and 2.48 for the Hispanic and Caucasian patients, respectively (P < 0.05)(4).

2. Family history
You are more likely to develop (more) kidney stones, if one the your directed family member have itor you already have them as a result of genetic factors, environmental exposures, or others(5).

3. Hyperuricemia
If you have hyperuricemia, you are at invreased risk to develop kidney stone as the result of the elevation of uric acid levels. Uric acid stones occur in 10% of all kidney stones and are the second most-common cause of urinary stones after calcium oxalate and calcium phosphate calculi(6).

4. Pregnancy
Although the risk is low, increased progesterone levels and decreased fluid intake during pregnancy may  be associated with the increased risk of the development of kidney stones. According to the study of 22,843 newborns or fetuses with CAs, 69 (0.30%) had mothers with KS during pregnancy. Of 38,151 matched control newborns without any abnormalities, 147 (0.39%) had KS during pregnancy. KS were associated with an adjusted prevalence odds ratio (POR) with 95% CI of 0.8, 0.6-1.0 for CAs(7).

5. Low urine pH (below 5.5) 
For uric acid crystallization and stone formation, low urine pH (below 5.5) is a more important risk factor than increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrheal states or severe dehydration(8).

6. Infection of urinary track
In the study of total of 100 kidney stone formers (59 males and 41 females) admitted for elective percutaneous nephrolithotomy who were recruited and microorganisms isolated from catheterized urine and cortex and nidus of their stones by Faculty of Associated Medical Science, Khon Kaen University, showed that from 100 stone formers recruited, 36 cases had a total of 45 bacterial isolates cultivated from their catheterized urine and/or stone matrices. Among these 36 cases, chemical analysis by Fourier-transformed infrared spectroscopy revealed that 8 had the previously classified 'infection-induced stones', whereas the other 28 cases had the previously classified 'metabolic stones'. Calcium oxalate (in either pure or mixed form) was the most common and found in 64 and 75% of the stone formers with and without bacterial isolates, respectively. Escherichia coli was the most common bacterium (approximately one-third of all bacterial isolates) found in urine and stone matrices (both nidus and periphery). Linear regression analysis showed significant correlation (r = 0.860, P < 0.001) between bacterial types in urine and stone matrices. Multidrug resistance was frequently found in these isolated bacteria. Moreover, urea test revealed that only 31% were urea-splitting bacteria, whereas the majority (69%) had negative urea test(9).

7. Water hardness 
In the study to evaluate whether the hardness of extra meal drinking water modifies the risk for calcium stones, showed that the main urinary risk factors for calcium stones, were measured in 18 patients with idiopathic nephrolithiasis, maintained at fixed dietary intake of calcium (800 mg/day), after drinking for 1 week 2 liters per day, between meals, of tap water and at the end of 1 week of the same amount of bottled hard (Ca2+ 255 mg/l) or soft (Ca2+ 22 mg/l, Fiuggi water) water, in a double-blind randomized, crossover fashion(10).

8. Obesity and diabetes
Obesity and diabetes were strongly associated with a history of kidney stones in multivariable models. The cross-sectional survey design limits causal inference regarding potential risk factors for kidney stones(11).

9. Etc.


III. Diagnosis
If you are experience tenderness over the back and groin or pain in the genital area without an obvious cause, it can be renal colic. After a complete physical examination and recorded family history, the most common test which your doctor order is CT scan.
1. CT scan and Ultrasound
The aim of CT scan is to detect the stones or obstruction within the urinary tract.In pregnant women, CT scan can be replaced by ultrasound to reduce the risk of radiation. Helical (also called spiral) computed tomography (CT) is considered as the best to locate and reveal the degree to which the stone is blocking the urinary tract. 

2. Urinalysis 
Urinalysis is important to detect blood or pus in the urine and determine whether or not symptoms are present.
According to the study by University of Chicago Pritzker School of Medicine, Current diagnostic evaluation of recurrent Ca oxalate nephrolithiasis should be conducted while the patients follow their usual diets and includes the following:
1. Analysis of stone composition by polarization microscopy.
2. Measurement of serum Ca, phosphate, uric acid, 1,25(OH)2D3, and creatinine.
3. Twenty-four-hour urine collection for an analysis of volume, pH, and excretion of Ca, phosphorus, magnesium, uric acid, citrate, sodium, oxalate, and creatinine(12).

IV. Prevention
The do's and do not list
1. Fluid intake, protein and sodium restriction, and thiazide will be effective in ICSFs and IPSFs by decreasing urine calcium concentration and CaOx and CaP SS and may also decrease plaque formation by increased PT calcium reabsorption. Citrate may be detrimental for IPSFs if urine pH rises greatly, increasing CaP SS. Future trials should examine the question of appropriate treatment for IPSFs(13).

2.  Moderate exercise
Moderate exercise to reduce the loss of fluid. If you involve in the extreme exercise, please remember to enough fluid to avoid dehydration.

3. Prevent vitamin overdose as they can cause the forming of kidney stones.

4. If you live in far North with water hardness, use water filter

5. If you are over weight or obese, lose weight

6. Reduced consumption of grapefruit juice cola drinks.
Study showed that grapefruit juice and cola drinks significantly (p=0.021) increased urinary excretion of citrate (25.8+/-9.3 vs 18.7+/-6.2 mg/h), calcium (6.7+/-4.3 vs 3.3+/-2.3 mg/h, p=0.015) and magnesium (2.9+/-1.5 vs 1.0+/-0.7 mg/h, p=0.003) and in the prevention of calcium renal stones a reduced sugar content is desirable to avoid the increase of urinary calcium due to the effect of sugar supplementation(14).

7. Drink more juices (organic)
Researchers at the University of Bonn, in the study of influence of grapefruit-, orange- and apple-juice consumption on urinary variables and risk of crystallization, indicated that due to an increased pH value and an increased citric acid excretion after consumption of each juice, the RSCaOx decreased statistically significantly (P<0.05) for grapefruit juice, but not significantly for orange and apple juice. The BONN risk index yielded a distinct decrease in the crystallization risk. We showed that both grapefruit juice and apple juice reduce the risk of CaOx stone formation at a magnitude comparable with the effects obtained from orange juice(15).

7. Increased intake of fruits with high in magnesium and potassium
Grapefruit juice significantly (p=0.021) increased urinary excretion of citrate (25.8+/-9.3 vs 18.7+/-6.2 mg/h), calcium (6.7+/-4.3 vs 3.3+/-2.3 mg/h, p=0.015) and magnesium (2.9+/-1.5 vs 1.0+/-0.7 mg/h, p=0.003). Citrus fruit juices could represent a natural alternative to potassium citrate in the management of nephrolithiasis(16).

8. Reduce intake of foods containing high amount of oxalate such as spinach, rhubarb, nuts, wheat bran, etc.

9. Others
According to the study of Dietary Factors and Risk of Kidney Stone: A Case-Control Study in Southern China, researchers at the Nanfang Hospital, Guangzhou, indicated that positive associations of kidney stones include consumption of grains (odds ratio [OR] = 2.08; 95% confidence interval [CI] = 1.08, 4.02) and bean products (OR = 3.50; 95% CI = 1.61, 7.59) in women. The variable "fluid drinking" showed a significant protective effect against kidney stones in men (OR = 0.57; 95% CI = 0.36, 0.88). Consuming leafy vegetables more than 3 times per day was positively associated with stones in both men and women (OR = 2.02; 95% CI = 1.04, 3.91 and OR = 3.86; 95% CI = 1.48, 10.04, respectively)(17).


V. Treatment
A. In conventional medicine perspective
Most kidney with diameter less than 5 mm (0.20 in) may pass through the urinary tract through urination within days of the onset of symptoms
A.1. Medications
The aims of medication is to manage pain or assist the speed up the spontaneous passage of ureteral calculi
1. Analgesia
Medication used to relieve pain.
2. Expulsion therapy
a. In the study to evaluate the efficacy of alfuzosin as medical expulsive therapy for distal ureteral stone passage od a total of 76 patients with a distal ureteral calculus, showed that the overall spontaneous stone passage rate was 75%, including 77.1% for placebo and 73.5% for alfuzosin (p = 0.83). Mean +/- SD time needed to pass the stone was 8.54 +/- 6.99 days for placebo vs 5.19 +/- 4.82 days for alfuzosin. (p = 0.003). There was no difference in the size or volume of stones that passed spontaneously between the placebo and alfuzosin arms, as measured on baseline computerized tomography (4.08 +/- 1.17 and 3.83 +/- 0.95 mm, p = 0.46) and by a digital caliper after stone expulsion (3.86 +/- 1.76 and 3.91 +/- 1.06 mm, respectively, p = 0.57). When comparing the improvement from the baseline pain score, the alfuzosin arm experienced a greater decrease in pain score in the days after the initial emergency department visit to the date of stone passage (p = 0.0005)(18).

A.2. Non invasive treatment and surgery
Extracorporeal shockwave lithotripsy does not require anaesthesia and requires little analgesia so that treatment can be given on an outpatient basis, and there is no wound to heal. Only a small puncture site is needed for percutaneous endoscopic lithotomy, and with the advent of prophylactic antibiotics there are few complications. Of renal stones, about 85% can now be successfully treated by extracorporeal lithotripsy alone, and almost all of the stones too large or hard for lithotripsy can be treated endoscopically, with ultrasonic or electrohydraulic probes being used to fragment the stone(19).

A.3. Recurrent treatments
2.1. Recurrent cystine renal stones
In the report of using ureterorenoscopy (URS) for the treatment of recurrent renal cystine stones. From 2003 to 2007, 10 patients (4 males and 6 females) with one or multiple recurrent renal cystine stones underwent URS. Overall, 21 procedures have been performed. Mean maximum diameter of stones was 11.2 mm (range 5-30 mm). Either 8-9.5 F semirigid or 7.9 F flexible ureteroscopes were used. In 6 cases, stones were removed using a basket; in 9 procedures laser lithotripsy with flexible scope was performed; in 6 cases renal calculi were pulled down in the ureter using flexible instrument and then shattered with laser introduced by semirigid instrument. Stone-free status was defined as the absence of any residual fragment. A complete stone clearance was obtained in 15 out of 21 procedures (71%). In 5 cases (24%) significant residual fragments occurred; in the remaining case (5%) URS was ineffective. In 5 out of these unsuccessful procedures, stone clearance was obtained with auxiliary treatments. The last patient has not been treated yet(20).

2.2. In general
Patients with kidney stones are highly motivated to prevent recurrence and were more amenable to fluid intake change than to another dietary or pharmaceutical intervention. Barriers preventing fluid intake success aligned into 3 progressive stages.
a. Stage 1 barriers included not knowing the benefits of fluid or not remembering to drink.
b. Stage 2 barriers included disliking the taste of water, lack of thirst and lack of availability.
c. Stage 3 barriers included the need to void frequently and related workplace disruptions.
Tailoring fluid intake counseling based on patient stage may improve fluid intake behavior(21).


B. In herbal medicine perspective
1. Asparagus racemosus Willd
In the study of the ethanolic extract of Asparagus racemosus Willd. for its inhibitory potential on lithiasis (stone formation), induced by oral administration of 0.75% ethylene glycolated water to adult male albino Wistar rats for 28 days, showed that the histopathological findings also showed signs of improvement after treatment with the extract. All these observations provided the basis for the conclusion that this plant extract inhibits stone formation induced by ethylene glycol treatment(22).

2. Goldenrod
Investigations in molecular pharmacology could show new mechanisms responsible for the biological effect of natural product from goldenrod extracts. The use of such herbal preparations with a rather complex action spectrum (anti-inflammatory, antimicrobial, diuretic, antispasmodic, analgesic) is especially recommended for treatment of infections and inflammations, to prevent formation of kidney stones and to help remove urinary gravel. This therapy is safe at a reasonable price and does not show drug-related side-effects, according to the study of the Institut für Pharmazie der Freien Universität Berlin, Berlin(23).

3. Other herbs
In the study of the effects of seven plants with suspected application to prevent and treat stone kidney formation (Verbena officinalis, Lithospermum officinale, Taraxacum officinale, Equisetum arvense, Arctostaphylos uva-ursi, Arctium lappa and Silene saxifraga) in female Wistar rats, showed that beneficial effects caused by these herb infusions on urolithiasis can be attributed to some disinfectant action, and tentatively to the presence of saponins. Specifically, some solvent action can be postulated with respect to uric stones or heterogeneous uric nucleus, due to the basifying capacity of some herb infusions. Nevertheless, for all the mentioned beneficial effects, more effective and equally innocuous substances are well known(24).

4. Etc.

C. In the traditional Chinese medicine perspective 
C.1. According to the article of Chinese medicine Hospital for Chronic and Difficult diseases(25), traditional Chinese medicine defined kidney stones is a condition caused by
1. Qi stagnation
a. The aim of the herbal treatment is to Promotethe circulation of qi, inducing diuresis, relieving strangury and removing the stones.
b. Herbal formula: Modified Pyrrosia Decoction 
Lysimachia, Pyrrosia leaf, Plantago seed, Cluster mallow fruit, Oriental water plantain rhizome, Citron fruit, Vaccaria seed, Radish seed and Rhubarb.
 
2. Damp-Heat Pattern
a. The aim of the herbal formula is to clear heat and dampness, relieve strangury and remove the stones.
b. Herbal formula: Modified Eight Health Restoring Powder
Lysimachia, Prostrate knotweed, Chinese pink herb, Talc, Phellodendron bark, Capejasmine fruit and Plantago seed , Rhubarb and Licorice root tip
  3. Kidney deficiency
a. The aim of the herb used to treat kidney stones as a result of kidney deficiency is to tonify qi, reinforce the kidney, relieve stranguria and remove the stones.  
b. Herbal formula: Modified Kidney-Reinforcing Decoction
Prepared rehmannia root, Wolfberry fruit, Dogwood fruit, Achyranthes root,  Bighead atractylodes. Rhizome eucommia bark, Cinnamon bark, Pilose asiabell root, Lysimachia and Climbing fern spore
 
C.2. Chinese herbal formula Wu Ling San (Poria, Rhizoma Alismatis, Polyporus, Cortex Cinnamomi, Rhizoma Atractylodis Macrocephalae (stir-baked))
In  the study to determine the effects of a traditional Chinese herbal formula, Wulingsan (WLS), on renal stone prevention using an ethylene glycol-induced nephrocalcinosis rat model. Forty-one male Sprague-Dawley (SD) rats were divided into four groups. Group 1 (n=8) was the normal control; group 2 (n=11) served as the placebo group, and received a gastric gavage of starch and 0.75% ethylene glycol (EG) as a stone inducer; group 3 received EG and a low dose of WLS (375 mg/kg); and group 4 received EG and a high dose of WLS (1,125 mg/kg), found that the rats of placebo group gained the least significant body weight; in contrast, the rats of WLS-fed groups could effectively reverse it. The placebo group exhibited lower levels of free calcium (p=0.059) and significantly lower serum phosphorus (p=0.015) in urine than WLS-fed rats. Histological findings of kidneys revealed tubular destruction, damage and inflammatory reactions in the EG-water rats. The crystal deposit scores dropped significantly in the WLS groups, from 1.40 to 0.46 in the low-dose group and from 1.40 to 0.45 in the high-dose group. Overall, WLS effectively inhibited the deposition of calcium oxalate (CaOx) crystal and lowered the incidence of stones in rats (p=0.035). In conclusion, WLS significantly reduced the severity of calcium oxalate crystal deposits in rat kidneys, indicating that Wulingsan may be an effective antilithic herbal formula(26).


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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/12649987
(1a) http://www.merckmanuals.com/home/kidney_and_urinary_tract_disorders/stones_in_the_urinary_tract/stones_in_the_urinary_tract.html?qt=&sc=&alt= 
(2) http://www.ncbi.nlm.nih.gov/pubmed/22218117
(3) http://www.ncbi.nlm.nih.gov/pubmed/20420802
(3a) http://www.ncbi.nlm.nih.gov/pubmed/22341269
(3b) http://www.ncbi.nlm.nih.gov/pubmed/15253722
(3c) http://www.ncbi.nlm.nih.gov/pubmed/6269684
(3d) http://www.ncbi.nlm.nih.gov/pubmed/10203369
(4) http://www.ncbi.nlm.nih.gov/pubmed/15865513
(5) http://www.ncbi.nlm.nih.gov/pubmed/9335385
(6) http://www.ncbi.nlm.nih.gov/pubmed/15493118
(7) http://www.ncbi.nlm.nih.gov/pubmed/17096158
(8) http://www.ncbi.nlm.nih.gov/pubmed/12649987 
(9) http://www.ncbi.nlm.nih.gov/pubmed/22461670
(10) http://www.ncbi.nlm.nih.gov/pubmed/9873217
(11) http://www.ncbi.nlm.nih.gov/pubmed/22498635 
(12) http://www.ncbi.nlm.nih.gov/pubmed/7671093
(13) http://www.ncbi.nlm.nih.gov/pubmed/21825103
(14) http://www.ncbi.nlm.nih.gov/pubmed/12408462
(15) http://www.ncbi.nlm.nih.gov/pubmed/12908889
(16) http://www.ncbi.nlm.nih.gov/pubmed/12408462
(17) http://www.ncbi.nlm.nih.gov/pubmed/22658934 
(18) http://www.ncbi.nlm.nih.gov/pubmed/18423747 
(19) http://www.ncbi.nlm.nih.gov/pubmed/8274898 
(20) http://www.ncbi.nlm.nih.gov/pubmed/21193905
(21) http://www.ncbi.nlm.nih.gov/pubmed/22341296
(22) http://www.ncbi.nlm.nih.gov/pubmed?term=asparagus%20root%20and%20kidney%20stones
(23) http://www.ncbi.nlm.nih.gov/pubmed/15638071
(24) http://www.ncbi.nlm.nih.gov/pubmed/7860196
(25) http://www.tcmtreatment.com/images/diseases/urinary-calculus.htm
(26) http://www.ncbi.nlm.nih.gov/pubmed/18040675