Biomedical subjects

Mary Ann Cameron

Publications and source records attributed to Mary Ann Cameron.

5 recordsLinked to original sources

PubMed2006

Urine composition in type 2 diabetes: predisposition to uric acid nephrolithiasis.

Type 2 diabetes is a risk factor for nephrolithiasis in general and has been associated with uric acid stones in particular. The purpose of this study was to identify the metabolic features that place patients with type 2 diabetes at increased risk for uric acid nephrolithiasis. Three groups of individuals were recruited for this outpatient study: patients who have type 2 diabetes and are not stone formers (n = 24), patients who do not have diabetes and are uric acid stone formers (UASF; n = 8), and normal volunteers (NV; n = 59). Participants provided a fasting blood sample and a single 24-h urine collection for stone risk analysis. Twenty-four-hour urine volume and total uric acid did not differ among the three groups. Patients with type 2 diabetes and UASF had lower 24-h urine pH than NV. Urine pH inversely correlated with both body weight and 24-h urine sulfate in all groups. Urine pH remained significantly lower in patients with type 2 diabetes and UASF than NV after adjustment for weight and urine sulfate (P < 0.01). For a given urine sulfate, urine net acid excretion tended to be higher in patients with type 2 diabetes versus NV. With increasing urine sulfate, NV and patients with type 2 diabetes had a similar rise in urine ammonium, whereas in UASF, ammonium excretion remained unchanged. The main risk factor for uric acid nephrolithiasis in patients with type 2 diabetes is a low urine pH. Higher body mass and increased acid intake can contribute to but cannot entirely account for the lower urine pH in patients with type 2 diabetes.

Adult↗

PubMed2005

Nephrolithiasis in children.

A metabolic etiology is the most common cause for pediatric kidney stones. Appropriate evaluation of affected children should include assessment of stone type, if available, and assessment of predisposing factors in all cases. This review discusses the metabolic disorders that lead to nephrolithiasis with respect to the development of calcium, uric acid, struvite, and cystine stones. Environmental and hereditary factors are summarized to provide a guide in the evaluation of pediatric stone formers.

Calcium↗

PubMed2004

Recurrent calcium nephrolithiasis associated with primary aldosteronism.

Typical manifestations of hyperaldosteronism include salt retention, hypokalemia, and metabolic alkalosis. However, a consequence infrequently recognized and described is hypocitraturia. In combination with hypercalciuria, aldosterone-induced hypocitraturia can trigger calcium nephrolithiasis. The authors report a case of an individual with primary hyperaldosteronism from an adrenal adenoma that resulted in hypocitraturia. The patient had severe recurrent renal calcium calculi that corrected with adrenalectomy. The clinical physiology of renal calcium and citrate handling in hyperaldosteronism is reviewed.

Adrenal Gland Diseases↗

PubMed2004

Minimal change disease with acute renal failure: a case against the nephrosarca hypothesis.

An unusual but well-documented presentation of minimal change disease is nephrotic proteinuria and acute renal failure. One pathophysiological mechanism proposed to explain this syndrome is nephrosarca, or severe oedema of the kidney. We describe a patient with minimal change disease who presented with heavy proteinuria and acute renal failure but had no evidence of renal interstitial oedema on biopsy. Aggressive fluid removal did not reverse the acute renal failure. Renal function slowly returned concomitant with resolution of the nephrotic syndrome following corticosteroid therapy. The time profile of the clinical events is not compatible with the nephrosarca hypothesis and suggests an alternative pathophysiological model for the diminished glomerular filtration rate seen in some cases of minimal change disease.

Acute Kidney Injury↗

PubMed2004

Novel insights into the pathogenesis of uric acid nephrolithiasis.

PURPOSE OF REVIEW: The factors involved in the pathogenesis of uric acid nephrolithiasis are well known. A low urinary pH is the most significant element in the generation of stones, with hyperuricosuria being a less common finding. The underlying mechanism(s) responsible for these disturbances remain poorly characterized. This review summarizes previous knowledge and highlights some recent developments in the pathophysiology of low urine pH and hyperuricosuria. RECENT FINDINGS: Epidemiological and metabolic studies have indicated an association between uric acid nephrolithiasis and insulin resistance. Some potential mechanisms include impaired ammoniagenesis caused by resistance to insulin action in the renal proximal tubule, or substrate competition by free fatty acids. The evaluation of a large Sicilian kindred recently revealed a putative genetic locus linked to uric acid stone disease. The identification of novel complementary DNA has provided an interesting insight into the renal handling of uric acid, including one genetic cause of renal uric acid wasting. SUMMARY: The recognition of metabolic, molecular, and genetic factors that influence urinary pH, and uric acid metabolism and excretion, will provide novel insights into the pathogenesis of uric acid stones, and open the way for new therapeutic strategies.

Circadian Rhythm↗