1/15. Prerenal azotemia in a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy.patients with hyporeninemic hypoaldosteronism show mild to moderate renal insufficiency, with a creatinine clearance of 20-75 ml/min, and asymptomatic hyperkalemia. A low degree of sodium wasting and mild hyperchloremic metabolic acidosis are also usually present. However, severe sodium wasting and volume depletion are not typically seen unless the patient is placed on severe sodium restriction or has some other cause of extrarenal sodium loss. In fact, acute renal failure has not been reported in such patients. We describe a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy who developed recurrent episodes of acute renal failure due to prerenal azotemia during acute exacerbations of diarrhoea. In our case, despite significant hypovolemia, the renin-aldosterone axis was markedly suppressed, implying that sympathetic tone played a decisive role in renin regulation.- - - - - - - - - - ranking = 1keywords = hyperkalemia (Clic here for more details about this article) |
2/15. Transient hyperkalemia and hypoaldosteronism in a patient with acute glomerulonephritis.The authors describe a 7-year-old boy with acute glomerulonephritis, who developed acute renal failure in the early course of his disease. While the renal function and other clinical manifestations gradually improved, hyperkalemia occurred unexpectedly, and returned to normal level spontaneously after a short period of symptomatic treatment. With the result of a low transtubular potassium gradient (TTKG) level, it was concluded that hypoaldosteronism was the major cause of hyperkalemia in this patient.- - - - - - - - - - ranking = 6keywords = hyperkalemia (Clic here for more details about this article) |
3/15. Transient hyporeninemic hypoaldosteronism in acute glomerulonephritis.While hyporeninemic hypoaldosteronism (HH) has been well described in relation to chronic renal diseases, transient HH has rarely been reported. Here we present a 9-year-old boy with acute glomerulonephritis who developed hyperkalemia, which persisted for a period of 3 weeks despite normal values of creatinine clearance and an absence of acidosis. He was diagnosed as having HH because of low basal plasma renin activity and serum aldosterone level. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis. There were no apparent pathological changes in the juxtaglomerular apparatus (JGA). Rapid adrenocorticotropic hormone administration increased adequately both serum aldosterone and cortisol levels. Responses of both plasma renin activity and serum aldosterone level following the furosemide upright provocation were blunted in the hyperkalemic acute phase, but recovered in the normokalemic convalescent phase. serum levels of human atrial natriuretic peptide were within normal range, both in the hyperkalemic and normokalemic phases. These results suggested that a transient dysfunction of the JGA, without volume expansion or structural damage of the JGA, caused HH in this patient.- - - - - - - - - - ranking = 1keywords = hyperkalemia (Clic here for more details about this article) |
4/15. cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases.BACKGROUND: Nephrotoxicity is a well-known effect of cyclosporine (CsA) that causes a reduction in glomerular filtration rate through vasoconstriction of the afferent glomerular arterioles and may result in acute renal failure. Isolated CsA-induced hyperkalemia occurring through different mechanisms is also common. However, there are only a few "case reports" addressing this phenomenon in allogeneic bone marrow transplantation patients. In this report, we propose mechanisms and methods of managing CsA-associated hyperkalemia in allogeneic transplantation. methods: We report on four allogeneic blood stem- cell transplant cases and a review of the literature. RESULTS: Four adult leukemia patients underwent allogeneic peripheral blood stem cell transplantation and received CsA as a part of their graft-versus-host disease prophylaxis. The patients developed hyperkalemia, despite adequate kidney function. CsA seemed to be the only pharmaceutical agent to which this electrolyte abnormality could be attributed. Renal tubule dysfunction and secondary hypoaldosteronism seemed to be the reasons for CsA-associated hyperkalemia. CONCLUSION: This report of four cases demonstrates that CsA should be considered among the possible causes of hyperkalemia in bone marrow transplantation. There may be a need for urgent intervention depending on the severity of hyperkalemia. Monitoring of blood CsA level and dose adjustment are important for the prevention of this complication.- - - - - - - - - - ranking = 10keywords = hyperkalemia (Clic here for more details about this article) |
5/15. Rare causes of acute hyperkalemia in the 1st week of life. Three case reports.We describe three neonates with hyperkalemia and renal salt wasting during the 1st week of life. Endocrinological evaluation led to the diagnosis of selective hypoaldosteronism (HA) in two neonates and secondary pseudohypoaldosteronism (PHA) in one. The infant with PHA developed a urinary tract infection, and radiological investigation demonstrated a small dysplastic left kidney with vesicoureteral reflux. The electrolyte and hormonal disturbances in this infant persisted throughout the first months of life. The two infants with selective HA improved rapidly after administration of fludrocortisone orally and the electrolytes and renin values returned to normal. Secondary PHA and selective HA should be considered in the differential diagnosis in salt-losing neonates during the first days of life. Renal ultrasonography, urine culture, and assays of aldosterone and plasma renin activity should be performed in any infant presenting with hyperkalemia and salt wasting after the exclusion of congenital adrenal hyperplasia.- - - - - - - - - - ranking = 6keywords = hyperkalemia (Clic here for more details about this article) |
6/15. Pseudo-hypo aldosteronism Type II.A 50-day-old infant diagnosed as meningitis had persistently elevated serum potassium, low serum bicarbonate and normal serum sodium. She had metabolic acidosis with low TTKG, low serum renin and low normal serum aldosterone with no renal failure or extra renal causes of hyperkalemia. Hence a diagnosis of Type II pseudo-hypoaldosteronism was made. She was started on oral thiazide following which her serum electrolytes normalized.- - - - - - - - - - ranking = 1keywords = hyperkalemia (Clic here for more details about this article) |
7/15. hyperkalemia after acute metabolic decompensation in two children with vitamin B12-unresponsive methylmalonic acidemia and normal renal function.The patients affected by vitamin B12-unresponsive methylmalonic acidemia (MMA) on the long run develop chronic renal disease with interstitial nephropathy and progressive renal insufficiency. The mechanism of nephrotoxicity in vitamin B12-unresponsive MMA is not yet known. Chronic hyporeninemic hypoaldosteronism has been found in many cases of methylmalonic acidemia, hyperkalemia and renal tubular acidosis type 4. We report 2 patients affected by B12-unresponsive methylmalonic acidemia diagnosed at the age of 23 months and 5 years, respectively, with normal glomerular filtration and function. They showed hyporeninemic hypoaldosteronism and significant hyperkalemia requiring sodium potassium exchange resin (Kayexalate) therapy after an episode of metabolic decompensation leading to diagnosis of MMA. In both children, hyporeninemic hypoaldosteronism and hyperkalemia disappeared after 6 months of good metabolic control.- - - - - - - - - - ranking = 3keywords = hyperkalemia (Clic here for more details about this article) |
8/15. pseudohypoaldosteronism: case report and discussion of the syndrome.A 41-year-old man, complaining of leg cramps, was found to have persistent hyperkalemia. Except for mild hypertension, his physical examination and laboratory values to exclude connective tissue diseases and diabetes mellitus were normal. Renal function testing revealed a normal glomerular filtration rate and tubular capacity to acidify and dilute, as well as near-normal ability to concentrate his urine. Hormonal evaluation revealed a normal cortisol, as well as normal resting and stimulated renin and aldosterone levels. A selective defect in tubular potassium secretion was demonstrated. In the absence of aldosterone deficiency or renal dysfunction, it was assumed that the patient had primary renal resistance to aldosterone, known as pseudohypoaldosteronism. Treatment with hydrochlorothiazide controlled his hyperkalemia and hypertension. His case emphasizes the diagnostic and therapeutic factors that should be considered in evaluating and treating a non-hospitalized patient with sustained hyperkalemia.- - - - - - - - - - ranking = 3keywords = hyperkalemia (Clic here for more details about this article) |
9/15. Reversible hyporeninemic hypoaldosteronism in a patient with tetraplegia.A 66-year-old man with tetraplegia developed hyperkalemia. Hyporeninemic hypoaldosteronism was disclosed on the basis of a lack of response of plasma renin activity to furosemide administration or tilting with marked hypotension and a subnormal response of aldosterone to furosemide stimulation, tilting, angiotensin ii infusion and ACTH administration, as well as increased vascular responsiveness to angiotensin ii infusion. Of interest was the finding that urinary excretion of epinephrine and norepinephrine was markedly reduced, indicating that hyporeninemia may possibly be due to a chronic lack of sympathetic nervous stimuli. The patient was treated with sodium polystyrene sulfonate resin and/or 9-alpha-fluorohydrocortisone, and wheelchair rehabilitation. However, even after stopping 8-month-mineralcorticoid replacement, normokalemia was maintained. Reexamination of the renin-angiotensin-aldosterone system revealed a normalized response to tilting or ACTH administration along with the normal catecholamine excretion. One more point to be noted is that ACTH administration resulted in a rise in the plasma levels of cortisol, corticosterone and 18-OH-corticosterone, but not aldosterone. This may be attributed to ACTH-stimulated 18-OH-corticosterone derived from the zona fasciculata or alternatively to a partial defect of corticosterone methyl oxidase type II (18-dehydrogenase) in the adrenal glomerulosa cells. These results suggested that hyporeninemic hypoaldosteronism may have been attributable to a decrease in systemic nervous stimuli and that such abnormalities were reversible.- - - - - - - - - - ranking = 1keywords = hyperkalemia (Clic here for more details about this article) |
10/15. captopril-induced metabolic acidosis with hyperkalemia.Hyperreninemic hypoaldosteronism was diagnosed in a 34-year-old woman with hypertension who was receiving captopril therapy. Renal biopsy revealed an advanced stage of IgA nephropathy, and her creatinine clearance was 40 ml/min. Elevation of serum potassium from 4.7 to 5.8 mEq/l and development of hyperchloremic metabolic acidosis with laboratory findings of pH 7.285, HCO3- 13.5 mEq/l, Na 141, and Cl 114 mEq/l were observed after captopril therapy. When captopril was withdrawn, elevated serum potassium levels and metabolic acidosis returned to normal. Challenge with captopril resulted in a decrease in plasma aldosterone levels, an increase in plasma renin activity, and development of hyperkalemic, hyperchloremic metabolic acidosis which is corrected with mineralocorticoid replacement. This case study demonstrates that captopril can cause hyperreninemic hypoaldosteronism with the laboratory finding of hyperkalemic, hyperchloremic metabolic acidosis.- - - - - - - - - - ranking = 4keywords = hyperkalemia (Clic here for more details about this article) |
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