Asymptomatic renal failure in a patient with bipolar disease without lithium therapy

A 48-year-old Chinese woman with a history of major depressionand bipolar disease, controlled by bromazepam, clozapine, fluoxepineand lamotrigine for several years, presented with microscopichaematuria (red blood cells: 10–25 per high power fieldon urinalysis) and acute renal failure (serum creatinine: 1.6mg/dL with a baseline value 0.8 mg/dL) upon routine health exam.She was referred to our hospital for further work-up. She deniedany previous ingestion of lithium. Neither analgesics nor anti-inflammatoryagents were used by the patient in the recent past. Her bodyweight (BW) was 71 kg. She showed no signs of dehydration, oedema,     

Proteinuria prevalence in insulin-treated patients: prediction of need for end-stage renal failure treatment

In the Dundee Diabetic clinic area (population circa 250,000), a population-based survey of the prevalence of proteinuria in diabetic patients treated with insulin showed that 9.4% of such patients had persistent proteinuria. The percentage of males with proteinuria was 11.4%, against 7.2% of females. An additional 5.2% of patients had proteinuria observed once, but did not meet the criteria for persistent proteinuria. No result was available in 10% of patients for a variety of reasons. Not every patient with diabetes and persistent proteinuria will progress to end-stage renal failure, but consideration of the group as a whole allows predictions based on published reports, to be made of the likely future incidence of renal failure, and hence future need for renal replacement services. We estimate that over the next decade two patients per 125,000 total population will develop renal failure each year. If survival is unchanged, there could be two or three times that number on treatment at any time.     

Development of Nephropathy in Diabetic Patients with a Single Kidney

Six diabetic patients with either a nephrectomy or a congenitally single kidney, and who later developed diabetic nephropathy, are described. They represent about 3 % of our diabetic population with nephropathy, and are the only patients in our clinic population known to have single kidneys. A reduced renal mass may augment the renal glomerular hyperfiltration associated with diabetes mellitus and increase the risk of later developing nephropathy.     

Diabetic renal disease in transitional and disadvantaged populations

SUMMARY: Diabetes mellitus has reached epidemic proportions throughout much of the world, and people from developing countries and disadvantaged groups from developed countries are affected disproportionately. Not only is diabetes more common in these populations, but it develops at an earlier age. Accordingly, patients have more years of life in which to develop the chronic complications of diabetes and the risk of complications is often further enhanced by limited access to health care. Renal disease is a frequent consequence of diabetes in these populations, and a number of factors related to poverty, malnutrition and accelerated lifestyle changes may lead to even greater rates in the future.     

Acute Oxalate Nephropathy Causing Late Renal Transplant Dysfunction Due to Enteric Hyperoxaluria

Calcium oxalate (CaOx) deposition in the renal allograft is an under recognized and important cause of acute tubular injury and early allograft dysfunction.
We present a case of late transplant dysfunction due to acute oxalate nephropathy. The patient presented with diarrhea and deteriorating graft function, and a diagnosis of enteric hyperoxaluria secondary to pancreatic insufficiency was made. This had occurred, as the patient had been noncompliant with his pancreatic enzyme replacement therapy. Treatment to reduce his circulating oxalate load was initiated, including twice-daily hemodialysis, low fat and oxalate diet and appropriate administration of pancreatic enzyme supplements. Graft function subsequently recovered.
The possibility of fat malabsorption leading to enteric hyperoxaluria should be considered in renal graft recipients presenting with loose stools and graft dysfunction.     

Predisposition to nephropathy in Polynesians is associated with family history of renal disease, not diabetes mellitus.

AIMS: Familial clustering of diabetes and nephropathy suggests that either common environmental or inherited mechanisms are important in developing diabetic nephropathy. If an inherited mechanism is important, the albumin excretion rate might be increased in those at future risk. This study aimed to determine whether people with a family history of diabetes or people with a family history of renal disease were most at risk. METHODS: In a two-by-two factorial study of urinary albumin in non-diabetic Polynesians, 90 people with a first degree relative (FDR) with end-stage renal failure (ESRF) and diabetes (group 1) were compared with 90 people with a FDR with non-diabetic ESRF (group 2), with 90 people with a FDR with diabetes but no known nephropathy (group 3) and 90 people with no known relatives with either diabetes or nephropathy (group 4). Groups were matched for ethnicity and age. RESULTS: Subjects with a family history of ESRF (groups 1 and 2) had an increased mean albumin-creatinine ratio (1.25 vs. 1.00 mg/mmol, P = 0.01), but in subjects with a family history of diabetes (groups 1 and 3), the mean ratios were not significantly different from those without a family history of diabetes (1.06 vs. 1.17 mg/mmol; P = 0.2). In those with a family history of nephropathy, fasting blood glucose and systolic blood pressure were increased, while fasting insulin and 2 h insulin concentrations were lower. A family history of diabetes was associated with an increased fasting blood glucose and 2-h blood glucose. By multiple linear regression, the mean systolic blood pressure (P = 0.02), the 2-h glucose concentration (P = 0.05), a family history of renal failure (P = 0.04), female sex (P = 0.0001) and the total cholesterol (P = 0.01) were each independently associated with microalbuminuria, while a family history of diabetes was not (P = 0.09). CONCLUSIONS: These data suggest that among Polynesians there is no specific inherited tendency to diabetic nephropathy per se. The risk of nephropathy does not appear to be associated with the degree of familial risk of diabetes itself. Rather, the risk of diabetic nephropathy may be the result of a familial risk of nephropathy from any cause and is associated with diabetes through relative hypoinsulinaemia and hyperglycaemia.     

Glycosylated haemoglobin in uraemia

Glycosylated haemoglobin (GHb) was measured in 71 patients with stable chronic renal failure by the thiobarbituric acid (TBA) reaction and by agar gel electrophoresis. Nineteen patients were diabetic. Of the non-diabetics, 22 were treated conservatively (including 8 children), 15 by maintenance haemodialysis, and 15 by continuous ambulatory peritoneal dialysis. GHb measured by both methods correlated with postprandial blood glucose levels. There was a significant discrepancy between the two methods only in patients with serum urea concentrations greater than 30 mmol/l, mean +/- SD, (6.8 +/- 2.6% vs 8.2 +/- 2.5% for TBA and electrophoresis, respectively). This difference, delta GHb, correlated with serum urea, serum creatinine, and serum bicarbonate, but after logistic regression of results from all 71 patients only serum urea was associated with delta GHb. Lower haemoglobin and GHb and high fetal haemoglobin concentrations in the haemodialysis group suggested increased haemolysis in these patients. Measurement of GHb by the TBA method and by agar gel electrophoresis remain useful indicators of hyperglycaemia in patients with mild, stable chronic renal failure.