Hyperkalemia in ambulant postcardiac surgery patients during combined therapy with angiotensin-converting enzyme inhibitor, spironolactone, and diet rich in potassium: A report of two cases and review of literature

Figures

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  Figure 1. Dietary K+ stimulates splanchnic receptors and causes aldosterone release which acts on principal cells of late distal convoluted tubule and cortical collecting duct that stimulates epithelial sodium channel which maintains electronegative environment by Na intake, favoring K+ secretion. It also stimulates 3Na+–2K+ ATPase, the renal outer medullary potassium and with-no-lysine kinase 4 channels that inhibit Na+–Cl− cotransporter in early distal convoluted tubule increasing delivery of Na, Cl in late distal convoluted tubule and cortical collecting duct hence providing substrate for epithelial sodium channel, increasing flow of urine that washes locally secreted K+ favoring more secretion. K+ directly increases expression of 3Na+–2K+ ATPase, the renal outer medullary potassium, epithelial sodium channel, and K+ maxi conductance channels

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  Figure 2. This figure shows K+ handling by the kidney. Proximal convoluted tubule: 65% K+ is reabsorbed. Thick ascending loop of Henle: K+ enters the cell via the Na+–K+–2Cl− cotransporter. Early distal convoluted tubule: Na+ and Cl− reabsorbed by Na+–Cl− cotransporter. K+ is secreted into the lumen via the renal outer medullary potassium channel. Late distal convoluted tubule, connecting tubule, and cortical collecting duct: (1) Principal cells: K+ secreted into the lumen by the renal outer medullary potassium channels and K+ maxi conductance channels. Epithelial Na channel shifts Na from the lumen to inside the cell. (2) Intercalated cells Type A: K+ taken up inside the cell from the lumen with the help of K+–H+ exchanger