Partial Urinary Tract Obstruction Research Articles

Could CA 19-9 be a useful biomarker in the diagnosis, prognosis, and prediction of adequate relief in lower urinary tract obstructions?

posterior urethral valves represent an important cause of childhood chronic kidney disease. The identification of biomarkers that indicate early kidney damage and even adequate clearance could reduce how many patients head towards kidney failure. this study evaluated how this easy-analysis biomarker (CA 19-9) could help identifying potential renal damage and adequate clearance in obstructive uropathies. 46 female Wistar rats were divided into 5 groups, with different patterns of partial urinary tract obstruction: group control; group OIV: infravesical obstruction; group OIVd: infravesical obstruction with reversion, obstruction relief 7 postoperative days later; group OUu: unilateral ureteral obstruction; group OUb: bilateral ureteral obstruction. The CA 19-9s performance was compared to another biomarker: Ngal. Determination of basal CA 19-9 and Ngal in urine and blood and serum creatinine levels was performed in the rats prior to surgery (T0) and after 14 days (T1). Group OIVd underwent intermediate (Ti) collection before clearance. the urinary concentration of CA 19-9 increased in groups OIV, OIVd and OUb; elevation at T1 and Ti, reached statistical significance compared to the T0 value (p<0,05). Changes in urinary CA 19-9 were more expressive in infravesical obstruction groups (AUC 0.81). Obstruction relief in group OIVd promoted significant urinary CA 19-9 reduction (p<0,05) in the final evaluation. CA 19-9 urinary concentration increased in partial urinary tract obstruction. Its best performance was in the bladder neck obstruction group, in which the elevation was detected early (6 days after infravesical obstruction) and the CA19-9 urinary concentration declined after clearance.

Salutary role for angiotensin in partial urinary tract obstruction

Salutary role for angiotensin in partial urinary tract obstruction.BackgroundIn the neonatal period, angiotensin II (Ang II) is up-regulated and induces a timely development of the renal pelvis and ureteral peristalsis, thereby protecting the kidney from hydronephrosis. We tested the possibility that in adulthood, Ang II may act salutarily on the kidney structure during partial urinary tract obstruction by inducing adaptive changes in the peristaltic machinery.MethodsAdult male Sprague-Dawley rats were subjected to partial unilateral ureteral obstruction (UUO) and divided into two groups, that is, those treated with (group L, N = 21) and those without (group C, N = 21) an angiotensin type 1 (AT1) receptor antagonist (losartan). Control animals were sham operated (N = 10). Rats were sacrificed either at day 7 or day 14.ResultsThe degree of hydronephrosis determined morphometrically was significantly more severe in group L than group C at both day 7 and day 14, indicating that Ang II inhibition accentuated hydronephrosis. The measurement of upstream pressure within the partially ligated ureter in vivo revealed that losartan significantly attenuates the frequency of ureteral peristaltic activities. In in vitro studies using ureteral strips harvested from normal adult Sprague-Dawley rats (N = 10), Ang II (10-8 mol/L) was shown to augment contraction, which was completely inhibited by losartan (10-6 mol/L).ConclusionsAng II has a salutary effect of protecting kidneys from hydronephrosis during partial ureteral obstruction through its ability to augment ureteral peristalsis. Salutary role for angiotensin in partial urinary tract obstruction. In the neonatal period, angiotensin II (Ang II) is up-regulated and induces a timely development of the renal pelvis and ureteral peristalsis, thereby protecting the kidney from hydronephrosis. We tested the possibility that in adulthood, Ang II may act salutarily on the kidney structure during partial urinary tract obstruction by inducing adaptive changes in the peristaltic machinery. Adult male Sprague-Dawley rats were subjected to partial unilateral ureteral obstruction (UUO) and divided into two groups, that is, those treated with (group L, N = 21) and those without (group C, N = 21) an angiotensin type 1 (AT1) receptor antagonist (losartan). Control animals were sham operated (N = 10). Rats were sacrificed either at day 7 or day 14. The degree of hydronephrosis determined morphometrically was significantly more severe in group L than group C at both day 7 and day 14, indicating that Ang II inhibition accentuated hydronephrosis. The measurement of upstream pressure within the partially ligated ureter in vivo revealed that losartan significantly attenuates the frequency of ureteral peristaltic activities. In in vitro studies using ureteral strips harvested from normal adult Sprague-Dawley rats (N = 10), Ang II (10-8 mol/L) was shown to augment contraction, which was completely inhibited by losartan (10-6 mol/L). Ang II has a salutary effect of protecting kidneys from hydronephrosis during partial ureteral obstruction through its ability to augment ureteral peristalsis.

Salutary role for angiotensin in partial urinary tract obstruction

In the neonatal period, angiotensin II (Ang II) is up-regulated and induces a timely development of the renal pelvis and ureteral peristalsis, thereby protecting the kidney from hydronephrosis. We tested the possibility that in adulthood, Ang II may act salutarily on the kidney structure during partial urinary tract obstruction by inducing adaptive changes in the peristaltic machinery. Adult male Sprague-Dawley rats were subjected to partial unilateral ureteral obstruction (UUO) and divided into two groups, that is, those treated with (group L, N = 21) and those without (group C, N = 21) an angiotensin type 1 (AT1) receptor antagonist (losartan). Control animals were sham operated (N = 10). Rats were sacrificed either at day 7 or day 14. The degree of hydronephrosis determined morphometrically was significantly more severe in group L than group C at both day 7 and day 14, indicating that Ang II inhibition accentuated hydronephrosis. The measurement of upstream pressure within the partially ligated ureter in vivo revealed that losartan significantly attenuates the frequency of ureteral peristaltic activities. In in vitro studies using ureteral strips harvested from normal adult Sprague-Dawley rats (N = 10), Ang II (10(-8) mol/L) was shown to augment contraction, which was completely inhibited by losartan (10(-6) mol/L). Ang II has a salutary effect of protecting kidneys from hydronephrosis during partial ureteral obstruction through its ability to augment ureteral peristalsis.

Phase-I Study of Protracted Infusion of Cisplatin

A continuous infusion schedule for cisplatin employing a portable infusion pump was studied in a phase-I trial designed to establish an optimal daily dose rate to deliver drug for protracted periods (up to 30 days). Fifteen trials were carried out in 14 patients at daily dose rates of 5, 6.5, 7.5, and 10.0 mg/M2 X day. The median duration of therapy at the respective doses was 21, 17, 8, and 7 days. Dose-limiting toxicity was recalcitrant and protracted nausea was observed in all patients receiving greater than 5 mg/M2 X day. One patient did develop mild thrombocytopenia (98,000) at day 35. Renal failure was relatively minor considering the absence of a concomitantly delivered hydration regimen but 3 patients did develop a transient rise in serum creatinine, 2 of whom had a solitary kidney or partial urinary tract obstruction. No patient developed renal failure at 5 mg/M2 X day. At the recommended dose of 5 mg/M2 X day, the cumulative dose of cisplatin delivered by a protracted infusion schedule is comparable to the intermittent high-dose regimen with less adverse drug complications.

Severe hypernatremia complicating urinary tract obstruction

Severe hypernatremia and hyperosmolar dehydration developed in a patient with partial urinary tract obstruction. The urine was initially hypotonic, and there was no response to exogenous vasopressin. These abnormalities resolved with relief of the urinary tract obstruction and replacement of the water deficit. This case documents lower urinary tract obstruction as a cause of nephrogenic diabetes insipidus and severe hypernatremia and illustrates its reversible nature.

Diuretic-Induced Renal Colic

To the Editor.— Two articles report 1,2 water- and beer-induced diuresis precipitating attacks of renal colic in patients with intermittent hydronephrosis. Here is an account of renal colic resulting from drug-induced diuresis. This response led to the discovery of previously asymptomatic partial urinary tract obstruction. Report of a Case.— A 43-year-old white woman with a uterine fibroid known since the age of 38, at an annual examination in 1972 complained of premenstrual edema with a weight gain of five pounds, tenderness of the breasts, and general body heaviness. No abdominal, back, or flank complaints appeared, nor had they on previous examinations dating back to 1960. Menstrual cycles were normal and not prolonged. A large irregular uterus extended into the right lower quadrant of the abdomen. A combination of 50 mg of triamterene (Dyrenium) and 25 mg of hydrochlorothiazide was prescribed every other morning beginning ten days before each period, as

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 . . .