Pathophysiology of renal concentrating defects

A number of advances which took place during the last decade have increased our understanding of the physiology and pathophysiology of urinary concentrating defects. The development of a highly sensitive radioimmunoassay for plasma vasopressin concentration has shed new light on vasopressin control mechanisms. The cellular action of vasopressin in biological membranes has been studied by various techniques. The role of adenylate cyclase, cyclic adenosine monophosphate (cAMP), microtubules, and microfilaments, in the response of vasopressin-sensitive membranes is now partially understood. New models of countercurrent multiplication systems, in which urea plays a prominent role, offer a better explanation of certain experimental facts. Such advances had permitted a better understanding of clinical conditions characterized by concentrating defects, including hyperkalemia, hypercalcemia, parenchymal renal disease, obstructive renal disease, and polyuria induced by certain drugs.