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The prevalence of urolithiasis has been increasing for the past few decades in industrialized nations. Uric acid calculi account for a significant percentage of urinary stones. Certain risk factors may be involved in the pathogenesis of uric acid nephrolithiasis, including hyperuricosuria, low urinary volume, and persistently low urinary pH. Patients with medical conditions that promote profound hyperuricosuria are at high risk of developing uric acid calculi. These conditions include chronic diarrheal states; myeloproliferative disorders; insulin resistance, including diabetes mellitus; and monogenic metabolic disorders, such as Lesch-Nyhan syndrome. Computed tomography can provide a definitive diagnosis. Except in cases in which there is severe obstruction, progressive azotemia, serious infection, or unremitting pain, the initial treatment of patients with uric acid nephrolithiasis should be medical dissolution therapy because this approach is successful in the majority of cases. A thorough review of the epidemiology and pathophysiology of uric acid nephrolithiasis is crucial for the diagnosis, treatment, and prevention of stones in patients with this condition.
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PMID:Uric Acid nephrolithiasis: recent progress and future directions. 1739 68

Bangladesh is one of the densely populated countries, a nation of 128 million people, 75% of whom lives in rural areas and the annual per capita gross national product (GNP) is US$ 380.00. The health care budget is 1.2% of GNP and the priority areas are population control, provision of clean drinking water and eradication of communicable diseases. The country has a small number of nephrologists and renal care is available in large cities only. The causes of renal diseases include glomerulonephritis, diabetes, hypertension, nephrolithiasis, obstructive uropathy and interstitial nephropathy. The incidence of end-stage renal disease is not known, but would be much higher than in developed countries because of high incidence of infection and environmental pollution. The treatment of ESRD has low priority in Bangladesh because of the government health policy and high cost of treatment. As a result, less than 10% of ESRD patients are able to maintain dialysis in private hospitals and governmental dialysis centers that are already overcrowded. The vast majority of patients who are started on dialysis die or stop treatment within the first three months. Renal transplantation is not as expensive as dialysis and is less costly in the university hospital than in private hospitals. Cyclosporine is usually replaced by azathioprine after six months of transplantation. Although organ act law is effective since 1998, cadaveric transplant has not picked up due to lack of infrastructure, facility and orientation regarding cadaveric transplantation. Preventive measures of renal disease can not be overemphasized.
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PMID:Health delivery system for renal disease care in bangladesh. 1764 75

The diagnosis of primary hyperparathyroidism (pHPT) is characterized by the constellation of elevated plasma serum calcium levels and low serum anorganic phosphate associated with inadequately high blood concentrations of parathyroid hormone (PTH). Parathyroid adenomas are the main reason for this disorder and can frequently be detected by ultrasound examination. Surgical removal of the parathyroid adenoma is recommended in the case of primary hyperparathyroidism complicated by osteoporosis, hyper-calciuria, nephrolithiasis, or impaired renal function. Here we present the case of a 68-year-old man with spontaneous remission of primary hyperparathyroidism two years after the diagnosis was established. The remission was documented by laboratory findings (normalisation of serum calcium and PTH levels) and by ultrasound examination that showed the disappearance of a cervical mass suggesting a parathyroid adenoma.
Exp Clin Endocrinol Diabetes 2007 Oct
PMID:Spontaneous remission of primary hyperparathyroidism. 1794 99

Kidney stones affect hypertensive patients disproportionately compared to normotensive individuals. On the other hand, some prospective data suggest that a history of nephrolithiasis was associated with a greater tendency to develop hypertension. Newer epidemiologic data also link obesity and diabetes, features of the metabolic syndrome, with nephrolithiasis. In this review, the association of hypertension, diabetes, and obesity with nephrolithiasis is reviewed, and possible pathogenic mechanisms are discussed. Patients with hypertension may have abnormalities of renal calcium metabolism, but data confirming this hypothesis are inconsistent. Higher body mass index and insulin resistance (i.e., the metabolic syndrome) may be etiologic in uric acid nephrolithiasis as increasing body weight is associated with decreasing urinary pH. The possibility that common pathophysiologic mechanisms underly these diseases is intriguing, and if better understood, could potentially lead to better therapies for stone prevention. Both hypertension and stones might be addressed through lifestyle modification to prevent weight gain. Adoption of a lower sodium diet with increased fruits and vegetables and low-fat dairy products, (for example, the dietary approaches to stop hypertension(DASH) diet), may be useful to prevent both stones and hypertension. In those patients in whom dietary modification and weight loss are ineffective, thiazide diuretics are likely to improve blood pressure control and decrease calciuria.
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PMID:The association of nephrolithiasis with hypertension and obesity: a review. 1821

Type 2 diabetes is associated with an increased risk of nephrolithiasis, specifically in the form of uric acid (UA) nephrolithiasis. Diabetic patients who produce uric stones exhibit a low urine pH, the key factor of UA crystallization. Production of such acidic urine appears to result from the insulin-resistant state characteristic of diabetes mellitus. Insulin resistance is also involved in the pathogenesis of primary UA nephrolithiasis observed in overweight subjects with the metabolic syndrome. Therefore, UA nephrolithiasis should be considered a possible manifestation of insulin resistance, as it already is for hyperuricemia. Occurrence of UA stones in a patient, especially if overweight or hypertensive, should prompt a search for components of the metabolic syndrome in order to implement therapeutic intervention aimed at preventing the development of type 2 diabetes and atherosclerotic complications. Reciprocally, diabetologists should be aware of the risk of UA stones in their patients.
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PMID:Diabetes and nephrolithiasis. 1825 8

Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is caused by mutations in SLC34A3, the gene encoding the renal sodium-phosphate co-transporter NaPi-IIc. Despite increased urinary calcium excretion, HHRH is typically not associated with kidney stones prior to treatment. However, here we describe two sisters, who displayed nephrolithiasis or nephrocalcinosis upon presentation. The index patient, II-4, presented with short stature, bone pain, and knee X-rays suggestive of mild rickets at age 8.5 years. Laboratory evaluation showed hypophosphatemia, elevated 1,25(OH) (2) vitamin D levels, and hypercalciuria, later also developing vitamin D deficiency. Her sister, II-6, had a low normal serum phosphorous level, biochemically vitamin D deficiency and no evidence for osteomalacia, but had undergone left nephro-ureterectomy at age 17 because of ureteral stricture secondary to renal calculi. Nucleotide sequence analysis of DNA from II-4 and II-6 revealed a homozygous missense mutation c.586G>A (p.G196R) in SLC34A3/NaPi-IIc. Ultrasonographic examinations prior to treatment showed grade I nephrocalcinosis for II-4, while II-6 had grade I-II nephrocalcinosis in her remaining kidney. Four siblings and the mother were heterozygous carriers of the mutation, but showed no biochemical abnormalities. With oral phosphate supplements, hypophosphatemia and hypercalciuria improved in both homozygous individuals. Renal calcifications that are presumably due to increased urinary calcium excretion can be the presenting finding in homozygous carriers of G196R in SLC34A3/NaPi-IIc, and some or all laboratory features of HHRH may be masked by vitamin D deficiency.
Exp Clin Endocrinol Diabetes 2009 Feb
PMID:Hypophosphatemic rickets with hypercalciuria due to mutation in SLC34A3/NaPi-IIc can be masked by vitamin D deficiency and can be associated with renal calcifications. 1852 28

Magnesium (Mg) is the main intracellular divalent cation, and under basal conditions the small intestine absorbs 30-50% of its intake. Normal serum Mg ranges between 1.7-2.3 mg/dl (0.75-0.95 mmol/l), at any age. Even though eighty percent of serum Mg is filtered at the glomerulus, only 3% of it is finally excreted in the urine. Altered magnesium balance can be found in diabetes mellitus, chronic renal failure, nephrolithiasis, osteoporosis, aplastic osteopathy, and heart and vascular disease. Three physiopathologic mechanisms can induce Mg deficiency: reduced intestinal absorption, increased urinary losses, or intracellular shift of this cation. Intravenous or oral Mg repletion is the main treatment, and potassium-sparing diuretics may also induce renal Mg saving. Because the kidney has a very large capacity for Mg excretion, hypermagnesemia usually occurs in the setting of renal insufficiency and excessive Mg intake. Body excretion of Mg can be enhanced by use of saline diuresis, furosemide, or dialysis depending on the clinical situation.
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PMID:Magnesium metabolism in health and disease. 1927 87

Idiopathic uric acid nephrolithiasis appears to be increasing in prevalence. While it has long been known that low urine pH is associated with uric acid stones, only recently has the pathophysiological basis for this disease emerged. Excessively acidic urine is the decisive risk for uric acid lithogenesis, and patients with diabetes and the metabolic syndrome often hold the company of low urine pH. While association does not imply causation, interesting insights have been made regarding insulin's influence on acid-base physiology. We review recent evidence from both the molecular and clinical realms to underline the importance of [H+] in the development and treatment of uric acid nephrolithiasis.
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PMID:Update on the pathophysiology and management of uric acid renal stones. 2042 21

Recent epidemiological studies revealed an association of obesity, diabetes mellitus, hypertension and metabolic syndrome (MetS) with kidney stone disease. We examined how these disorders cause kidney stones. A clinical study on 467 patients with nephrolithiasis at our institution revealed that clustering of MetS traits increased the risk of uric acid stone formation by decreasing urinary pH. A subsequent study analyzing detailed data from 30,448 patients enrolled in the 6th Nationwide Survey on Urolithiasis in Japan showed that clustering of MetS traits were associated with an increased severity of the kidney stone disease and elevated urinary excretion of calcium, uric acid and oxalate. Finally, the OLETF rats, an animal model of MetS, showed lower urinary pH, decreased citrate excretion, and increased uric acid and calcium excretion. In addition, the administration of pioglitazone, an agent that improves insulin resistance, significantly increased the urinary pH. These results indicate that MetS causes changes in urinary constituents, leading to an increased risk of both uric acid and calcium oxalate stone formation. We suggest that kidney stone disease should be considered as a component of MetS and that the improvement in insulin resistance by means of diet and lifestyle changes and medical therapy might help to prevent this disorder.
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PMID:[Metabolic syndrome and nephrolithiasis]. 2130 61

Nephrolithiasis research and care have been focused on biochemical changes in urinary solute excretion leading to stone formation, but abnormalities in urine chemistry alone do not explain many aspects of the condition of patients with kidney stone disease. Evidence exists of an association with metabolic syndrome, obesity, diabetes and hypertension, and of enhanced risk of chronic kidney disease and metabolic bone disease. Very recently also a higher risk of cardiovascular events and damage has been reported in kidney stone formers when compared with non-stone formers. It is time to view nephrolithiasis as a condition predictive of chronic kidney disease and cardiovascular damage, which deserves full metabolic evaluation together with an early prevention care strategy, mainly consisting of dietary and lifestyle changes, in a multidisciplinary approach. Kidney stone disease should be considered as a systemic disorder with clinical relevance beyond symptomatic urinary tract obstruction.
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PMID:Update on nephrolithiasis: beyond symptomatic urinary tract obstruction. 2162 79


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