Hyporeninemic hypoaldosteronism hyperkalemia

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. 

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from large clinical trials indicated above show that only 1.5% of patients treated with ACE inhibitors or ARBs were withdrawn from trials because of hyperkalemia, and no deaths were reported as a consequence of hyperkalemia.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. 

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... 

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