1/16. IgA nephropathy in a patient with polycythemia vera. Clinical manifestation of chronic renal failure and heavy proteinuria.IgA nephropathy (IgAN) is one of the most frequent forms of glomerulonephritis (GN). However, its association with polycythemia vera (PV) has rarely been described. We report a case of IgAN combined with PV. The patient was a 46-year-old male with chronic renal failure, heavy proteinuria and erythrocytosis. He also presented hypertension and hematuria as well as splenomegaly, high arterial oxygen saturation and elevated leukocyte alkaline phosphatase activity. Possible causes of secondary erythrocytosis were ruled out. The renal biopsy revealed mesangial proliferative GN with predominant IgA deposition in mesangium. He was diagnosed as having IgAN and PV concomitantly. After administration of hydroxyurea, enalapril and felodipine, blood cell count and blood pressure normalized, while azotemia persisted. There was also a partial remission of the heavy proteinuria. We describe a case of IgAN associated with PV, and possible pathophysiologic relationships between two diseases are discussed with review of the literature.- - - - - - - - - - ranking = 1keywords = azotemia (Clic here for more details about this article) |
2/16. Allograft diabetic nephropathy may progress to end-stage renal disease.Mesangial expansion and glomerular basement membrane thickening characteristic of diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed end-stage renal disease (ESRD) due to recurrent diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of proteinuria, uncontrolled hypertension, azotemia, renal allograft pathologic findings and the need for hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed glucose metabolism pre-transplantation. The three patients presented had different varieties of diabetes; type 1, type 2 and new onset diabetes after transplantation (NODAT). In each subject, proteinuria was detected by dipstick at a mean of 8.3 yr (range 8-9) post-transplantation and increased to the nephrotic range (3.7-4.8 g/day) inducing hypoalbuminemia and azotemia. A histopathologic diagnosis of allograft diabetic nephropathy was made in a mean of 11.7 yr (range 10-14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis, arteriolosclerosis, and tubular atrophy with marked tubular basement membrane thickening characteristic of advanced diabetic nephropathy. All three patients manifested uremia and resumed hemodialysis. Two patients died from sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance hemodialysis. We infer that recurrent or de novo diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of ESRD due to allograft diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression.- - - - - - - - - - ranking = 2keywords = azotemia (Clic here for more details about this article) |
3/16. role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.- - - - - - - - - - ranking = 1keywords = azotemia (Clic here for more details about this article) |
4/16. germanium dioxide-induced nephropathy: a new type of renal disease.Chronic renal failure developed in 5 patients who were taking germanium dioxide (GeO2)-containing compounds. Renal functional deterioration was slow but progressive and dialysis treatment was necessitated temporarily in 2 patients. After the discontinuation of GeO2, the impaired renal function tended to improve but remained abnormal for an observation period of 10-40 months. The lack of proteinuria and hematuria was characterized as the clinical manifestations. Renal biopsy specimens revealed the tubular epithelial cell degeneration containing hematoxylin-positive fine granules on light microscopy, and electron-dense inclusions in the swollen mitochondria on electron microscopy. These findings localized mainly in distal segment of the tubules. In the rats given GeO2 orally for 10 weeks, similar histological lesions were evident, as manifested by marked weight loss, anemia, azotemia, and negative proteinuria. In the rats given carboxyethylgermanium sesquioxide, these changes were not observed and Ge concentration of kidney was significantly lower than in the rats given GeO2. The present study indicates that chronic GeO2 intake causes progressive renal dysfunction characterized by the degeneration of distal tubules.- - - - - - - - - - ranking = 1keywords = azotemia (Clic here for more details about this article) |
5/16. Renal failure associated with vesicoureteral reflux.In a review of over 600 charts with a major diagnosis of vesicoureteral reflux only 21 were found to have coexisting azotemia. Nine of 11 patients treated surgically with technically successful operations had either improvement or stabilization of their renal function. All such cases had moderate degrees of azotemia (creatinine of less than 3.5 mg. per 100 ml.). Surgery is recommended in cases of gross reflux and in cases with evidence of parenchymal damage, before deterioration in renal function has become irreversible.- - - - - - - - - - ranking = 2keywords = azotemia (Clic here for more details about this article) |
6/16. Pre-renal azotemia mimicking chronic renal failure in a hypotensive patient.A 56-year-old Samoan man with a documented history of hypertension, who presented with atrial fibrillation and hypotension, quickly developed renal failure with a serum urea nitrogen of 1.370 g/L and a serum creatinine of 92 mg/L. After hydration of the patient, the creatinine value became normal in two days, the urea nitrogen in four days. The urinary creatinine output during the first 24 h of hospitalization was 3.7 g. This case illustrates the rapidity with which unusually large amounts of creatinine (more commonly seen in chronic renal failure) can accumulate and be excreted in pre-renal failure. It also reaffirms the usefulness of the urea nitrogen/creatnine ratio in evaluating the causes of azotemia.- - - - - - - - - - ranking = 5keywords = azotemia (Clic here for more details about this article) |
7/16. Perinatal asphyxia and renal failure in neonatal patients.Herein we discuss oliguria and azotemia in neonatal patients associated with perinatal complications, including difficult labor and delivery, and respiratory asphyxia. Renal failure in these patients is accompanied by proteinuria, microscopic hematuria and red blood cell casts, and it generally resolves in 7 to 10 days. Umbilical aortography can be helpful in determining the presence of normal kidneys in these patients.- - - - - - - - - - ranking = 1keywords = azotemia (Clic here for more details about this article) |
8/16. histoplasmosis with hypercalcemia, renal failure, and papillary necrosis. confusion with sarcoidosis..A 56-year-old man with a three-month history of fever, malaise, anorexia, mental confusion, and weight loss had hypercalcemia and azotemia. The chest roentgenogram was normal. biopsy material removed 2 1/2 years previously showed noncaseating granulomas. sarcoidosis was diagnosed, and prednisone was administered. fever persisted, and the patient died 49 days after admission. Postmortem examination showed evidence of extensive disseminated histoplasmosis, interstitial nephritis, and papillary necrosis. This communication emphasizes the difficulty in diagnosing the etiology of disseminated, noncaseating granulomatous disease.- - - - - - - - - - ranking = 1keywords = azotemia (Clic here for more details about this article) |
9/16. Kappa light chain nephropathy without evidence of myeloma cells. Response to chemotherapy with cessation of maintenance hemodialysis.A rarely diagnosed nodular glomerulopathy is presented arising secondary to kappa light chain deposition and clinically characterized by hypertension, congestive heart failure, massive proteinuria and slowly progressive azotemia. Kappa light chains were detected in the urine, the glomerular nodules, and the basement membranes of both glomeruli and tubules. A malignant proliferation of plasma cells could not be detected. Two morphologic features were unusual: the presence of microaneurysms, and the deposition of immunoglobulin and complement in a similar pattern to the kappa light chains. Noteworthy clinical aspects included the elusiveness of the proper diagnosis, the massive proteinuria in the absence of amyloid deposits, and the remarkable improvement in renal function following intermittent chemotherapy.- - - - - - - - - - ranking = 1keywords = azotemia (Clic here for more details about this article) |
10/16. Chronic renal insufficiency from cortical necrosis induced by arsenic poisoning.A 39-year-old man had anuria and azotemia and was found to be suffering from acute arsenic poisoning. After two peritoneal dialyses, partial renal function returned, and the patient has survived for five years without dialysis. Renal cortical necrosis was demonstrated by renal biopsy and renal calcification. We suggest that arsenic be added to the list of substances capable of causing renal cortical necrosis and recommend consideration of this complication in cases of arsenical poisoning.- - - - - - - - - - ranking = 1keywords = azotemia (Clic here for more details about this article) |
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