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At least 235 records · Page 13Linked to original sources
PubMed1992

Radiographic and serologic correlates of azotemia in patients with posterior urethral valves.

A retrospective statistical analysis with a minimum followup of 10 years was done on 102 patients who presented in early childhood with posterior urethral valves. All patients were treated with initial bladder drainage. Factors correlating with the development of renal failure were evaluated. No patient with a normal kidney on 1 side had renal failure. Calculated glomerular filtration rate was significantly higher in patients who retained adequate renal function (80.7 +/- 17.8 ml. per minute per 1.73 m.2), as compared with those who had renal failure (18.6 +/- 9.6 ml. per minute per 1.73 m.2). Patients with renal failure also had a significantly higher serum creatinine level at stabilization (2.0 +/- 0.8 mg./dl.) than those who had adequate renal function (0.5 +/- 0.2 mg./dl.). The presence of bilateral high grade vesicoureteral reflux, hydronephrosis and nonfunction was significantly higher in patients with renal failure. Patient age at presentation was not a significant factor. These data represent a guideline for the prognosis and management protocols of infants with dilated upper urinary tracts and posterior urethral valves.

Age Factors↗
PubMed1999

Transplantation, not dialysis, corrects azotemia-dependent priming of the neutrophil oxidative burst.

The oxidative burst of neutrophils from patients with renal failure before the initiation of dialysis is primed for an enhanced response after stimulation by phagocytosis or chemoattractants. This study shows that phagocytosis-stimulated oxidative burst activity remains primed in patients treated with both high-efficiency hemodialysis and continuous ambulatory peritoneal dialysis (CAPD), but it is normal in patients with a functioning renal transplant. Incubation of normal neutrophils or HL-60 granulocytes in azotemic plasma results in increased resting and phagocytosis-stimulated H2O2 production, which is rapidly reversible on removal of the plasma. Priming of the oxidative burst by azotemic plasma is independent of changes in opsonization and phagocytosis and does not require protein synthesis. These results suggest that azotemic plasma contains a substance or substances capable of reversibly priming oxidative burst activity in neutrophils and neutrophil-like cell lines. The Inability of high-efficiency hemodialysis and CAPD to normalize oxidative burst activity suggests that this substance is of higher molecular weight.

Adult↗
PubMed1987

Contribution of the urea appearance rate to diuretic-induced azotemia in the rat.

Studies were performed to evaluate the contribution of the urea appearance rate to the elevated plasma urea concentration found during diuretic-induced sodium depletion. Negative sodium balance of -1162 + 29 microEq/100 g body wt was induced over a four day period by the administration of furosemide, 20 to 30 mg/kg/d i.p., to rats ingesting a sodium free diet. When compared with sodium replete controls, sodium depletion significantly increased the plasma urea concentration (65.0 +/- 3.1 vs. 26.4 +/- 1.1 mg/dl) through both an increase in the urea appearance rate (160 +/- 5.2 vs. 125 +/- 3.5 mg/day/100 g body wt), and a decrease in the urea clearance rate (1.99 +/- 0.14 vs. 3.16 +/- 0.12 ml/min/kg). The urea appearance rate increased on the first day of diuretic administration, remained elevated three days after stopping diuretics, rapidly returned to control levels after sodium repletion, and was significantly correlated with the magnitude of sodium deficit. Similar results were obtained when diuretic-induced sodium depletion was produced in adrenalectomized animals. After four days of sodium depletion the plasma concentration was increased for some amino acids but not for the plasma total amino acid, nitrogen concentration. The results indicate that sodium depletion increases the urea appearance rate through a mechanism that is independent of adrenal function. Thirty to sixty percent of the elevation in plasma urea concentration that occurs in the rat during diuretic-induced sodium depletion can be accounted for by an enhanced urea appearance rate.

Adrenalectomy↗
PubMed2003

Treating azotemia-induced anemia with erythropoietin improves diabetic eye disease.

BACKGROUND: Coincidental with the pandemic growth of diabetes as the prime cause of end-stage renal disease (ESRD), blindness attributable to diabetic retinopathy has become a major concern for all those involved in the care of diabetic ESRD patients. Vision loss is linked to progression of proliferative retinopathy and macular edema. METHODS: Extracted from a study of azotemic anemic pre-ESRD patients treated with erythropoietin, a cohort of five diabetic subjects was reassessed in terms of stability of renal function, changes in blood rheology, and course of diabetic eye disease. RESULTS: All subjects reported subjective improvement in well-being, including enhanced effort tolerance following an increase in hematocrit from a baseline level of to 29.6 +/- 2.0% to a level of 39.5 +/- 2.4% after one year of treatment with erythropoietin (P = <0.0005). Neither hypertension nor deterioration of renal function was noted in any subject. Three patients with macular edema evinced substantive improvement-based stable vision and documented resolution noted in flourescein angiography. CONCLUSION: Erythropoietin treatment of anemic azotemic diabetic patients is well tolerated. In a small observational retrospective study of three patients with macular edema, retention of vision and resolution of exudates was noted.

Anemia↗
PubMed1986

[Familial proximal tubular azotemia. Elevated urea plasma levels in normal kidney function].

A family showed a renal disturbance, characterized by an elevated urea plasma concentration while glomerular filtration was found to be normal. A detailed study of renal clearance was performed on two members of this family in order to define the nature and site of the disorder. Evidence points to an isolated impairment of urea elimination, giving rise to a reduced urea concentrating ability and thus to a decrease in maximum urine concentration and water conservation. The most probable site of this impairment seems to be the proximal tubule.

Adult↗