Hypoaldosteronism hyporeninemic

Treatment with angiotensin-converting enzyme inhibitors is also more likely to be associated with hyperkalemia in older individuals (69). Impaired angiotensin II formation limits this potent stimulus for aldosterone secretion, and this is superimposed on the already age-related decrease in activity of the renin-angiotensin-aldosterone axis. The same drug-induced hyporeninemic hypoaldosteronism is predicted for the angiotensin receptor blockers. However, to date this has not been documented clincally. 

Bonnet F, Thivolet CH. Reversible hyperkalemia at the initiation of ACE inhibitors in a young diabetic patient tvith latent hyporeninemic hypoaldosteronism. Diabetes Care 1996 19(7) 781. 

Kalin ME, Poretsky E, Seres DS, Zumoff B. Hyporeninemic hypoaldosteronism associated with acquired immune deficiency syndrome. The American journal of medicine. 1987 May 82(5) 1035-8. 

ACE inhibitors and ARBs slow the progression of diabetic kidney disease. A trial that was reported in 2000 confirmed that even nonmicroalbuminuric type 2 diabetic patients should be managed with ACE inhibitors or ARBs to prevent cardiovascular events.In addition to lowering systemic blood pressure, such patients also have lowered glomerular capillary blood pressure and protein filtration,ACE inhibitors and ARBs also reduce All-medi-ated effects on glomerular permeability and cell proliferation and fibrosis and should be incorporated into the treatment schedules of all patients with type 2 diabetes and those with type 1 diabetes and microalbuminuria, ACE inhibitors may exacerbate hyperkalemia in patients with advanced CKD and/or hyporeninemic hypoaldosteronism. In older patients with renal artery stenosis, they may cause a rapid decline in kidney function. Pooled data from large clinical trials indicated above show that only 1.5% of patients treated with ACE inhibitors or ARBs were withdrawn from trials because of hyperkalemia, and no deaths were reported as a consequence of hyperkalemia. ... 

Selective Aldosterone Deficiency (Type IV RTA). In type IV RTA, there is failure of distal potassium and hydrogen ion secretion because of aldosterone deficiency or resistance. This may occur because of a range of steroid or steroid receptor synthetic defects or because of hyporeninemic hypoaldosteronism (e.g., due to diabetic nephropathy, tubulointerstitial disease, urinary obstruction, renal transplantation, or SLE). Hyperkalemia, although mild, is a usual manifestation. 

Interpretation Responses must be defined for the assay technique used. Patients with renin-dependent forms of hypertension (e.g., renovascular hypertension) show values that are approximately five times normal. Stimulated responses are also seen in patients with high-renin essential hypertension, pheochromocytoma, and Barttei s syndrome. Patients with hypertension firom mineralocorticoid excess (e.g., primary aldosteronism) usually have PRA below the concentration of assay sensitivity. Patients with hyporeninemic hypoaldosteronism usually have low concentrations of plasma renin and low aldosterone concentrations. Figure 51-17 shows typical responses. 

Hyperkalemic distal (type IV) RTA resulting from generalized distal tubule defects is less common than hyporeninemic hypoaldosteronism, but is more common than classic distal (type I) RTA. Patients with this defect have impaired tubular potassium secretion in addition to impaired urinary acidification (urine pH >5.5 despite acidemia or acid loading). Urinary obstruction is the most frequent cause of this disorder, which may also be associated with sickle-cell nephropathy, systemic lupus erythematosus, HIV nephropathy, analgesic abuse nephropathy, amyloidosis, renal transplant rejection, and chronic cyclosporine nephrotoxicity. 

Just why is plasma prorenin activity elevated in diabetics An explanation can be offered in the finding that in adult diabetics administered furosemide, large increases in plasma prorenin activity are seen, especially in those subjects with albuminuria, and plasma renin activity is below the normal range. Thus, it would appear that the efficiency of the conversion of prorenin to renin is affected in diabetics, with the effect being more severe in diabetics with hyporeninemic hypoaldosteronism (67). 

There is also clear evidence that the sequel of lead inducing a chronic nephropathy with hypertension can occur. At times, this hypertension may be sufficiently severe to be malignant and may precipitate an early demise [22]. In more chronic cases, the hypertension may be of moderate degree and not be sufficient to cause progressive deterioration of renal function [43]. However, when confronted with a patient with hypertension and mild renal damage, it can be difficult to determine which came first and particularly difficult to determine whether lead was a contributor to the renal damage that caused the hypertension. In such cases, the hypertensive mechanism would be the same as those associated with other varieties of chronic renal disease. By contrast, many patients with chronic lead nephropathy have demonstrated suppressed plasma renin concentrations indicative of a hyporeninemic hypoaldosteronism [44]. 

Tan, S.Y., Shapiro, R., Stockard, H. and Mulrow, P.J. (1979). Indomethacin-induced prostaglandin inhibition with hyperkalemia. A reversible cause of hyporeninemic hypoaldosteronism. Ann. Intern. Med., 90, 783-85... 

Renal tubular acidosis can be classified into two main types, type I and type II, which are hereditary (11). Renal tubular acidosis can also result from accumulation of waste products, including a variety of metabolic acids in uremia. Another type of renal tubular acidosis, type IV, is due to hyporeninemic hypoaldostero-nism. Hypoaldosteronism appears to be secondary to the inability of the kidney to... 

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