Post-obstructive Diuresis Research Articles

Hypomagnesemia following the diuresis of post-renal obstruction and renal transplant.

Three unusual cases are described which demonstrated hypomagnesemia and symptoms resembling magnesium deficiency syndrome. The hypomagnesemia was most likely secondary to urinary losses from diuresis following release of post-renal obstruction and renal homotransplantation. Heretofore, this association has not been described. Case 1 was unique because of the post-obstructive diuresis in the face of marked renal impairment. Case 2 is noteworthy because of the profound hypomagnesemia, 0.4 mEq/1, and because of the development of congestive heart failure. The rapid improvement noted in cardiac function with magnesium replacement suggests a relationship to magnesium deficiency.

Renal sodium- and potassium-activated adenosine triphosphatase deficiency during post-obstructive diuresis in the rat.

Renal function studies and tissue enzyme analysis were carried out in rats with bilateral ureteral ligation (24 h) and after relief of obstruction at intervals of 2 h, 24 h, 3 days, and 7 days. A persistent decrease in glomerular filtration rate and in tubular reabsorption of sodium, solute, and water was noted at each interval after relief of obstruction. Renal sodium- and potassium-activated adenosine triphosphatase (Na–K-ATPase) activity was unchanged in kidneys obstructed for 24 h, but enzyme activity was decreased in the outer medulla of the kidney and, less often, in the renal cortex, at each interval studied during the post-obstructive period. Magnesium-dependent adenosine triphosphatase (Mg-ATPase) activity was not changed in any of the groups. In the post-obstructive kidney (24 h, 3 days, and 7 days) there was a significant correlation between the decrease in outer medullary Na–K-ATPase activity and the changes in filtered sodium load, tubular reabsorption of sodium, and urine osmolality. A deficiency of renal Na–K-ATPase could be important in the pathogenesis of post-obstructive natriuresis and diuresis.

Postobstructive diuresis: Studies in a dialyzed patient with a solitary kidney

Urinary excretion was studied in a volume-expanded, dialyzed patient who experienced a profound diuresis after passage of a uric acid calculus which had obstructed the ureter of his solitary horseshoe kidney. Natriuresis (23 per cent of the filtered load of sodium at peak flow) was accompanied by massive urinary losses of water, potassium, magnesium, calcium, bicarbonate, phosphate and uric acid. The data suggest that inhibition of proximal tubular reabsorptive processes was the major factor producing diuresis. Persistent free water clearance and initial potassium secretion indicate that the function of the distal tubule was largely intact. This diuretic pattern in association with retained ability to modulate sodium excretion after completion of diuresis suggests that volume expansion was the primary cause of blockade to proximal tubular reabsorption. Recommendations are made for the clinical management of the patient with diuresis after relief of obstruction.

Diagnosis, Characterization and Management of Post-obstructive Diuresis

Diagnosis, Characterization and Management of Post-obstructive Diuresis

Defect in proximal and distal sodium transport in post-obstructive diuresis

Defect in proximal and distal sodium transport in post-obstructive diuresis. Bilateral urinary obstruction was created in rats by tying a ligature around the bladder below the ureteral orifices. Sham-operated rats served as controls. Water intake was limited and food was withheld from both groups during and following obstruction. Release of the obstruction after 30hr was followed by a diuresis lasting 24 to 36hr. One group of rats was kept in balance cages before, during and after obstruction. After release of the obstruction, experimental animals had lower creatinine clearance and higher urine flow, Na, K and solute excretion than did sham-operated controls. Urine flow in the experimental animals exceeded water intake during the postobstructive period. A second group of rats was prepared identically and used for clearance and micropuncture measurements beginning 14hr after release of the obstruction. Plasma concentrations of K, urea and total solutes were elevated. C In was reduced and V, U Na V, U K V, U Osm V and C Osm were elevated. Na and water reabsorption were reduced in the proximal and distal nephron, distal K secretion was increased, and a marked defect in concentrating ability was present. The reduction in proximal Na reabsorption was not associated with a reduced peritubular capillary protein concentration. Tracer microinjection experiments with a third group of rats revealed abnormal permeability to mannitol and inulin. The defect in Na reabsorption is probably due to an increased backflux of Na, reducing net Na reabsorption. GFR is probably not identical to inulin or creatinine clearance in post-obstructive diuresis.

Micropuncture study of chronic obstructive nephropathy before and after release of obstruction

Micropuncture study of chronic obstructive nephropathy before and after release of obstruction. The nature of the intrinsic renal defect in chronic obstructive nephropathy was studied in rats with unilateral partial ureteral ligation. In the surface nephrons of chronically hydronephrotic kidneys, proximal intratubular pressure was slightly increased when compared to sham-operated control animals. Tubular fluid flow rate was reduced by 35%, fractional reabsorption was increased by 8% and single nephron filtration rate was 76% of control values. There was no post-obstructive diuresis in rats with a normal contralateral kidney studied 2 to 6 hrs after relief of chronic obstruction and there was no evidence of hyperfiltration or decreased fractional reabsorption in the proximal tubule of surface nephrons in the post-obstructive kidney. A disproportionately high surface nephron to whole kidney glomerular filtration rate (GFR) was present in most animals studied before or after relief of obstruction. It is concluded that the increased fractional excretion of sodium and diminished urine osmolality observed in chronic obstructive nephropathy result from decreased reabsorption in the distal nephron and/or impaired function of the deep nephrons and renal medulla. The results also indicate that these intrarenal functional defects are not solely responsible for the phenomenon of post-obstructive diuresis; it must also depend on other factors such as superimposed volume expansion or further reduction in functioning nephron mass.

A micropuncture study of postobstructive diuresis in the rat.

In order to investigate the syndrome of postobstructive diuresis, clearance and micropuncture studies were carried out in rats after relief of 24 hr of bilateral (BUL) or unilateral (UUL) ureteral ligation. In rats with BUL, a striking diuresis and natriuresis occurred when the obstruction to one kidney (the experimental kidney) was relieved. The results were not influenced by administration of vasopressin or d-aldosterone. Whole kidney clearances of inulin and p-aminohippuric acid (PAH) in the experimental kidney were reduced to 10% and 20% of normal, respectively. Superficial nephron inulin and PAH clearances were also reduced, but only to 40% and 45%, respectively. These findings suggest a heterogeneity of nephron function in which deep nephrons were functioning poorly or not at all. To investigate the site of impaired tubular reabsorption in the surface nephrons, absolute and fractional water reabsorption was measured. Absolute reabsorption was found to be decreased all along the nephron. Fractional reabsorption in proximal tubules was normal, as indicated by an average endproximal tubular fluid per plasma inulin (TF/P(In)) of 2.16 vs. 2.30 in controls. TF/P(In) was markedly decreased in distal tubules (2.91 vs. 8.02) and final urine (5.56 vs. 263). These observations indicate that the major sites of impaired sodium reabsorption leading to the diuresis were beyond the proximal tubule.Rats with 24 hr of UUL did not demonstrate a comparable natriuresis or diuresis either spontaneously when the obstruction was relieved or after i.v. infusion of urea. A major difference between the BUL and UUL rats was that prerelease intrarenal hydrostatic pressure was markedly elevated (30.1 mm Hg) in the former but was below normal free-flow values (9.2 mm Hg) in the latter. Thus, elevation of intrarenal pressure during the period of obstruction may be causally related to the natriuresis and diuresis which occurs after the obstruction is relieved.

Hypernatremia complicating partial urinary-tract obstruction.

IT is well known that the ability of the kidneys to concentrate urine is impaired by obstruction of the urinary tract.1 2 3 Nephrogenic diabetes insipidus4 5 6 7 has been shown to occur both with partial Urinary Tract obstruction and in the course of postobstructive diuresis after relief of complete urinary-tract obstruction. That severe hypernatremia and hyperosmolar dehydration may occur in certain patients with partial urinary-tract obstruction, however, is not generally appreciated. Thus, a recent review of hypernatremia8 and two standard textbook chapters9 , 10 on obstructive uropathy do not describe this phenomenon. The course of two illustrative patients seen over the past five years with . . .