Renal Acidification in Patients with Mineralocorticoid Deficiency

Pérez, Guido O.; Oster, James R.; Vaamonde, Carlos A.

doi:10.1159/000180754

Cited by 27 publications

(12 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…are similar to those reported by other authors [7,[9][10][11][12]. In this group we observed a close inverse expo nential correlation between urinary sodium levels and PRA (r = 0.908; p < 0.001).…”

Section: Discussionsupporting

confidence: 92%

“…4) (r = 0.588; p < 0.05), both under basal conditions and after a NH4C1 overload. This correlation is similar to that described in other alterations in renal acidification [12,60,61], in which the decrease in NH4 secretion leads to an alkalinization of the urine. Di Telia et al [53], working with adrenalectomized rats subjected to an NH4C1 overload, reported results consistent with our own.…”

Section: Discussionsupporting

confidence: 89%

See 1 more Smart Citation

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

Villoria

Núñez²,

Miralles³

et al. 1988

Am J Nephrol

View full text Add to dashboard Cite

Plasma renin activity, plasma aldosterone levels and renal tubular capacity to excrete hydrogen ions were studied in 13 patients suffering from diabetes mellitus with a creatinine clearance of less than 40 ml/min. The results were compared with those obtained in a control group, in a group of nondiabetic subjects with chronic renal failure (CRF) and in a group of diabetic patients without CRF. Twelve of the thirteen diabetic patients with CRF had data characteristic of hyporeninemic hypoaldosteronism associated with type IV renal tubular acidosis. On comparing the results with those of the other two groups of patients, it was observed that the manifestations of the latter two groups considered separately were different from those of the problem group, although in the diabetic patients with normal glomerular filtration rate (GFR) hyporeninism but not hypoaldosteronism was present accompanied by a lower net acid excretion (p < 0.001) due to a lower excretion of NH₄ (p < 0.05) and titratable acid (p < 0.001) when the patients were challenged with an NH₄C1 overload. We believe that a conjunction of diabetes and renal failure is necessary for the diabetic patients with a decrease in GFR to show hyporeninemic hypoaldosteronism and type IV tubular acidosis.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 89%

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

Villoria

Núñez²,

Miralles³

et al. 1988

Am J Nephrol

View full text Add to dashboard Cite

show abstract

“…Nevertheless, effective circulating volume depletion could also have played a role in the significant increase in serum potassium concentration [4], Even though scrum chloride levels were within normal limits, a relative hyperchlor emia (serum NaVCF = 1.33) was apparent. The presence of hyperchloremic metabolic acidosis in our patient was probably the result of (a) a loss of aldosterone effect at the outer medullary collecting duct, (b) a dimin ished phosphate excretion from lack of glu cocorticoid and (c) a depression of ammoniagenesis by hyperkalemia [5][6][7], Finally, hypercalcemia was also present in our pa tient, possibly owing to adrenal insufficiency [ 8],…”

mentioning

confidence: 50%

Polyglandular Autoimmune Syndrome Presenting as Acute Renal Failure with Severe Hyperkalemia

Elisaf¹,

Pappas²,

Siamopoulos³

1996

Nephron

View full text Add to dashboard Cite

“…In addition to hypoaldosteronism, a reduction in the number of nephrons would be ex pected to amplify a reduction in net acid excretion by limiting renal ammonia production and by impairing bicarbonate reabsorption [13,14].…”

Section: Discussionmentioning

confidence: 99%

Captopril-Induced Metabolic Acidosis with Hyperkalemia

Sakemi¹,

Ohchi²,

Sanai³

et al. 1988

Am J Nephrol

View full text Add to dashboard Cite

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/1 and development of hyperchloremic metabolic acidosis with laboratory findings of pH 7.285, HCO^-₃13.5 mEq/1, Na 141, and CI 114 mEq/1 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.

show abstract

Renal Acidification in Patients with Mineralocorticoid Deficiency

Cited by 27 publications

References 16 publications

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

Polyglandular Autoimmune Syndrome Presenting as Acute Renal Failure with Severe Hyperkalemia

Captopril-Induced Metabolic Acidosis with Hyperkalemia

Contact Info

Product

Resources

About