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[Desobstructive sodium and water diuresis: pathophysiologic and clinical aspects of bilateral obstructive nephropathy (author's transl)].

The measurement of sodium and water loss after relieve of the obstruction shows that the obstructive nephropathy originates in three pathogenetic mechanisms. (1) Acute complete bilateral ureteric obstruction causes tubular atrophy, prevents both resorption and glomerular filtration, reduces the renal blood flow and increases the extracellular space by retention of water and products subject to urinary excretion. (2) Relieve of obstruction results in excess polyuria as blood flow and glomerular filtration recover rapidly, the extracellular space gets rid of its osmotic load, and the tubular dysfunction of resorption continues for several days until the epithelium has recovered from its pressure atrophy. All this will result in a high loss of sodium and water which requires adequate substitution; otherwise, natriuretic shock will result. (3) The chronic (bilateral) obstruction behaves in a similar way, yet is less reversible. The tubular damage is the same. Moderate polyuria occurs already during the stage of obstruction. Hereby the extracellular space decreases. After relieve of the obstruction the polyuria increases significantly, yet less rapidly than after acute obstruction as the glomerular function does not recover completely. The renal blood flow remains diminished, the vascular calibers stay narrowed, and the kidney remains shrunken. Loss of sodium and water will endanger the patient with chronic obstruction. Furthermore, the patient will be at risk due to dehydration, acidosis, anemia and uremia. The infusion therapy of the desobstructive nephropathy syndrome is based upon the venous pressure and the serum electrolytes which are measured twice daily.