[Diagnosis and pathophysiology of renal concentration disorders]

Basic physiology and pathophysiological mechanisms of renal concentrating ability and its defects are discussed. Normal urinary concentration depends on the concerted action of a variety of factors. Consequently, many different causes may underly the symptom of polyuria. Clinical tests of concentrating ability (water deprivation, pitressin test) are of diagnostic importance in diabetes insipidus and polydipsia, but have little practical value in the work-up for chronic renal disease. A critical analysis of maximal concentrating capacity (TcH2O) during induced osmotic diuresis is conducted. It is inferred that the height and shape of the normal TcH2O curve results basically from two physiological processes: It is raised by increasing NaCL transport out of the medullary parts of the ascending limbs of Henle's loops and lowered by influx of hypotonic tubular urine into the collecting ducts. Preponderance of hypotonic influx may result in hypotonic final urine in the absence of tubular functional abnormalitiy. It is not appropriate, therefore, to classify renal concentrating defects according to the shape and height of the TcH2O curve. A synopsis and short description of the known renal concentrating defects is given. They are classified into hereditary, metabolic, diuretic-induced, and toxic disturbances, as well as those seen in renal disease of various etiology. Each defect is discussed in terms of the underlying pathophysiological mechanism as far as currently understood. The most important mechanisms are either disturbed NaCL transport in the ascending limb of Henle's loop, or antidiuretic hormone (ADH) dependent or ADH independent decrease in water permeability of the enddistal convolutions and collecting ducts, or osmotic diuresis.