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PubMed1987

Toxicity of amphotericin B plus flucytosine in 194 patients with cryptococcal meningitis.

A multicenter prospective randomized trial of four versus six weeks of amphotericin B, 0.3 mg/kg per day, plus flucytosine, 150 mg/kg per day, was performed with 194 patients with cryptococcal meningitis. One or more toxic drug reactions developed in 103 patients: azotemia (51), renal tubular acidosis (two), leukopenia (30), thrombocytopenia (22), diarrhea (26), nausea/vomiting (10), and hepatitis (13). The four- and six-week regimens were complicated by toxicity in 44 percent and 43 percent of cases, respectively. Toxicity appeared during the first two weeks of therapy in 56 percent and during the first four weeks in 87 percent. Azotemia did not occur more frequently in renal transplant recipients or diabetic patients. Cytopenias did not appear more often in patients with hematologic malignancies or those receiving immunosuppressive therapies. Toxic reactions that contributed to death developed in five patients (two with azotemia, one with pancytopenia, one with hepatitis, one with ileus). Amphotericin B-induced azotemia was not a significant risk factor for the subsequent development of bone marrow, gastrointestinal, or hepatic toxicity attributable to flucytosine. Flucytosine toxicity was associated with peak serum flucytosine levels of 100 micrograms/ml or more during two or more weeks of therapy (p = 0.005). Peak 5-fluorouracil levels were not predictive of toxicity. An initial dose of flucytosine is recommended based on the creatinine clearance: 150 mg/kg per day at a creatinine clearance above 50 ml/minute, 75 mg/kg per day at a creatinine clearance of 26 to 50 ml/minute, and 37 mg/kg per day at a creatinine clearance of 13 to 25 ml/minute. The serum creatinine level should be monitored twice weekly and the creatinine clearance weekly during therapy in order to anticipate changes in serum flucytosine concentration. In addition, it is recommended that the serum flucytosine level be determined two hours after an oral dose once a week, and that the dose be adjusted to maintain a level of 50 to 100 micrograms/ml.

Adolescent↗

PubMed2000

Treatment and outcome of dogs with leptospirosis: 36 cases (1990-1998).

OBJECTIVE: To characterize serologic and clinical features and outcome of dogs with leptospirosis that were treated conservatively (i.e., medical management alone) or with hemodialysis. DESIGN: Retrospective study. ANIMALS: 36 dogs with leptospirosis. PROCEDURE: History; results of physical examinations, ultrasonography, and serologic, hematologic, and serum biochemical analyses; time to resolution of azotemia; and outcome were obtained from medical records. Dogs were treated conservatively (n = 22) or with hemodialysis (14). RESULTS: Between 1990 and 1998, amount of rainfall was positively correlated with number of cases of leptospirosis identified per year. Serum antibodies against 6 Leptospira serovars were measured, and titers were highest to Leptospira pomona in 16 (44%) dogs, L bratislava in 9 (25%) dogs, and L hardjo in 1 (3%) dog. Eight (22%) dogs had equally high titers to L pomona and L bratislava, 1 (3%) had equally high titers to L grippotyphosa and L canicola, and 1 (3%) had high titers to L grippotyphosa, L pomona, L canicola, and L bratislava. During initial evaluation, all dogs were azotemic. Thirty (83%) dogs survived, including 12 of 14 (86%) dogs treated with hemodialysis and 18 of 22 (82%) treated conservatively. Serum creatinine concentration was similar in both groups after resolution of clinical signs. CONCLUSIONS AND CLINICAL RELEVANCE: Infection with L pomona and L bratislava was recognized as a cause of leptospirosis in dogs, and resulted in development of acute renal failure with various degrees of azotemia. Prognosis for dogs with mild to moderate azotemia was good with conservative treatment, whereas treatment with hemodialysis appeared to improve prognosis for dogs with severe azotemia.

Animals↗

PubMed1980

The effect of hemodialysis on levels of cyclic nucleotide-associated hormones in patients with chronic renal failure.

In order to determine the molecular basis for the loss of catecholamine responsiveness in skeletal muscle in chronic azotemia, plasma and serum levels of catecholamines and other hormones whose mechanisms of action are associated in part with cyclic nucleotide mediation were assessed in 37 patients with chronic azotemia. Samples were obtained prior to and immediately following conventional hemodialysis. Plasma epinephrine and norepinephrine levels in patients predialysis were increased 50% and 25% respectively compared to control subjects. Levels of insulin, prolactin, aldosterone and renin were also in creased in azotemic patients prior to dialysis. Conventional hemodialysis reduced serum levels of growth hormone, but had no effect of the elevated levels of all other hormones found in patients predialysis. In particular, plasma epinephrine and norepinephrine levels were unaffected by hemodialysis. Despite these findings, hemodialysis did reduce to normal levels the elevated plasma levels of cyclic AMP and cyclic GMP observed in uremic subjects predialysis. These data are consistent with increased adrenergic outflow in patients with chronic azotemia, and suggest a mechanism of homologous desensitization of the catecholamine receptor adenylyl cyclase unit in chronic azotemia.

Aldosterone↗

PubMed2005

Late onset renal failure from angiotensin blockade (LORFFAB): a prospective thirty-month Mayo Health System clinic experience.

BACKGROUND: Worsening azotemia following initiation of angiotensin blockade (AB), in patients with CKD, RAS with/without precipitating factors is recognized. Small increases in serum creatinine following initiation of AB occur and must not warrant drug discontinuation. We anecdotally had observed improvement in CKD in patients with normal renal arteries and no precipitating factors, following termination of AB. The worldwide ESRD epidemic, coincident with increasing use of AB, prompted us to hypothesize a late-onset azotemia in such CKD patients. MATERIAL/METHODS: Over 30 months, 103 patients with worsening azotemia, while on AB were evaluated. Ninety-seven patients with abnormal MRA and/or with precipitating factors were excluded. In the remaining five, AB was discontinued, and GFR monitored. RESULTS: One male, four females, mean age 66.2 years. Three diabetic/hypertensives, one SLE/hypertensive, one diabetic/kidney transplant recipient. Mean stable AB, 25.2 months, (6-66 months). Mean follow up, 11.8 months. One month following discontinuation of AB, GFR increased by a mean 45%. Mean serum creatinine decreased from 2.9+/-0.9 to 1.8+/-0.4 mg/dL (p=0.04). Uremic symptoms in 3, hyperkalemia in one, secondary hyperparathyroidism in one, resolved. Two with anemia, now require less erythropoietin. CONCLUSIONS: We called this unrecognized potentially reversible late-onset worsening azotemia, occurring several months to years on stable AB, in CKD patients with normal renal arteries, without precipitating factors, late-onset renal failure from angiotensin blockade (LORFFAB). Pathophysiologically, the concept of microvascular RAS is invoked. The extent of LORFFAB, with millions of patients worldwide on AB, remains conjectural and warrants further investigation.

Aged↗

PubMed2006

[Chronic renal disease and gravidity--case study].

Uremia, the result of renal failure, is a serious clinical problem. Rising azotemia during gravidity significantly increases perinatal morbidity and mortality. This study presents the case of 34 years old patient with 27-year medical history of diabetes mellitus type 1 with diabetic nephropathy and chronic renal insufficiency. The patient got pregnant in the stage of preterminal renal failure. During the first trimester, she showed hypertension and proteinuria. In her 25th week of pregnancy, she was hospitalized with progressive proteinuria, almost uncontrollable hypertension and increased azotemia. Intensive conservative therapy led to a slight decrease of azotemia and proteinuria levels which, however, remained high. In fact, we considered using elimination methods several times. Due to severe hypoxia of the foetus, the gravidity was terminated by section at 30 weeks. After the parturition, the newborn had to be resuscitated. In the first days, the newborn showed increased azotemia which decreased spontaneously after several days. In a month after the termination of gravidity, N-substances increased again and the patient was enrolled in the chronic dialysis programme.

Adult↗

PubMed1991

Aspirin injection test to predict angioplasty outcome in unilateral renovascular hypertension: preliminary report.

We examined the usefulness of aspirin DL-lysine for prediction of the outcome of renal artery angioplasty in renovascular hypertension. The study was carried out in eight hypertensive patients with unilateral renal artery stenosis: six were free from azotemia and two had slight azotemia. Before and 30 min after an intravenous injection of aspirin DL-lysine (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin E2 and plasma renin activity. Blood pressure and heart rate were serially measured at this time. Renal angioplasty was later performed and was technically successful in all patients. In the six patients without azotemia, aspirin inhibited renal prostaglandin E2 synthesis and suppressed renin release from the ischemic kidney, resulting in lowered blood pressure. Renal angioplasty caused plasma renin activity to become normal and lowered high blood pressure. The reduction in blood pressure by angioplasty was correlated with the responses of blood pressure and renin release to aspirin. However, in the two patients with azotemia, aspirin neither suppressed renin release nor lowered blood pressure. Their hypertension was not reduced by the angioplasty. These results indicate that an aspirin injection test could be useful for prediction of the outcome of angioplasty in unilateral renovascular hypertension.

Adult↗

PubMed1987

Acute renal failure.

Acute renal failure is divided into its classic parts: prerenal azotemia, postrenal azotemia (obstruction), and renal azotemia (including acute tubular necrosis). The division of acute tubular necrosis into the ischemic and toxic varieties is supplemented by an analysis of toxic varieties into those caused by antibiotics, radiologic contrast agents, chemotherapeutic-immunosuppressive agents, heavy metals, organic solvents, etc. Acute tubular necrosis caused by hemoglobin and myoglobin is described in detail. The importance of urinalysis and the urinary indices in distinguishing prerenal azotemia from acute tubular necrosis is stressed. Finally, current prognosis and treatment are reviewed.

Acute Kidney Injury↗

PubMed1988

Surgical management of renal trauma: analysis of risk factors, technique, and outcome.

The impact of the extent of renal injury and the method of treatment on patient outcome has not been well defined. Ninety-two patients with 96 renal injuries treated by a variety of surgical methods were evaluated to determine whether outcome was influenced by the extent of renal injury (minor, major, vascular, or bilateral) or the method of treatment (exploration alone, renorrhaphy, partial nephrectomy, nephrectomy, vascular repair, combined surgery, or bilateral surgery). Each patient was assessed for the extent of associated injury (injury score, transfusion requirement), the presence of shock, degree of hematuria, type of injury and method of repair, incidence of major complications, and azotemia (creatinine greater than 1.5 mg/dl). Eight patients died, ten developed azotemia, and 35 developed a major complication. There was a statistically significant association between the extent of injury and the development of azotemia. A statistically significant relationship was noted between the type of repair (nephrectomy, combined and bilateral surgery) and the development of azotemia, major complication and eventual death. These relationships, however, seemed to be a product of the extent of associated injury and consequent development of sepsis and multiple organ failure rather than the extent of renal injury or the method of repair.

Adolescent↗

PubMed1984

Urinary chloride concentration in acute renal failure.

The present prospective study was undertaken to evaluate the usefulness of urinary chloride concentration in determining the cause of an abrupt decline in renal function. 99 patients from diverse clinical settings with multiple causes of acute renal failure were evaluated. Urinary chloride concentrations of less than 20 mEq/l were observed in most cases of reversible prerenal azotemia (20 of 21 cases) and were observed in more frequently than urinary sodium concentration of less than 20 mEq/l (13 of 21 cases, p less than 0.01). Only prerenal azotemia accompanying diuretic use was associated with high urinary chloride concentrations (57 +/- 7 mEq/l). When prerenal azotemia occurred in the setting of metabolic alkalosis with bicarbonaturia, urinary chloride was low (4.0 +/- 1.0 mEq/l) while urinary sodium was high (65.0 +/- 19.0 mEq/l). In patients with oliguric and nonoliguric acute tubular necrosis, and in patients with acute exacerbations of chronic renal failure, mean urinary chloride concentration ranged from 40 to 67 mEq/l and mean fractional excretions of chloride ranged from 7.2 to 8.4%. Only 11% of patients with oliguric and nonoliguric acute tubular necrosis had urinary chloride concentrations of less than 20 mEq/l. Urinary chloride concentrations exhibited greater sensitivity and equivalent specificity as urinary sodium concentrations in differentiating patients with reversible prerenal azotemia from those with oliguric and nonoliguric acute tubular necrosis.

Acidosis↗

PubMed1978

beta2-Microglobulin in Balkan endemic nephropathy.

The results of low molecular weight (LMW) proteinuria test in urines of patients and suspect subjects in an endemic area of Balkan endemic nephropathy (BEN) in Yugoslavia are reported. An accordance between the positive LMW test and the clinical diagnosis of BEN has been found in more than 70%. The authors claim that LMW immunodiffusion test is a very useful procedure for detecting BEN and a great aid in the epidemiological work in the endemic field. The results of determining beta2-microglobuline (beta2m) in serums and urines by radioimmunoassay technique as well as counting of clearances of endogenous creatinine in healthy persons, "endangered" subjects in endemic area, and BEN patients without azotemia, with azotemia and uremia are reported. The group of 17 patients suffering of BEN without azotemia having slightly or more markedly lowered creatinine clearances showed higher serum and much higher urinary concentration of beta2m which are not in proportion with creatinine clearance. The results are interpreted so far as a consequence of the predominant tubular lesion in BEN. In groups of patients with azotemia and uremia no differences in beta2m handling have been found. The report has a preliminary character and requires further study.

Beta-Globulins↗

PubMed1981

Serious hyponatremia in patients with cancer: management with demeclocycline.

Seventeen patients with cancer or aplastic anemia received demeclocycline as treatment for hyponatremia. Prior to demeclocycline therapy no patients showed clinical signs of fluid overload or saline depletion. In all patients inappropriately concentrated urine (mean urine osmolality = 548 mOSM/kg H2O) or increased urine content of sodium (mean urine sodium = 91 mEq/L) were documented prior to demeclocycline therapy. No patient had developed hyponatremia in association with antineoplastic drug therapy. The average serum sodium (NaS) at the time of initiation of therapy was 121 mEq/L. NaS increased in all patients despite the simultaneous administration of generous volumes of fluid. NaS exceeded 130 mEq/L and average of 3.5 days following institution of demeclocycline. Patients lost an average of 2.3 kg during demeclocycline. The toxicity noted following demeclocycline was azotemia and increased serum creatinine. Eight patients developed serum urea nitrogen (SUN) in excess of 25 mg/dl; average maximum creatinine in these eight patients was 1.9 mg/dl. Average peak creatinine in eight patients who did not develop azotemia was 0.87 mg/dl. Azotemia seemed to be correlated with simultaneous administration of other nephrotoxic agents and with administration of higher doses (1200 mg/day) of demeclocycline.

Creatinine↗

PubMed1980

Acute tumor lysis syndrome. A review of 37 patients with Burkitt's lymphoma.

Renal and metabolic complications of tumor lysis during 46 episodes of remission induction chemotherapy were reviewed in 37 patients with American Burkitt's lymphoma. Azotemia occurred in 14 patients, preceding chemotherapy in eight. All of these patients had abdominal tumors. Pretreatment azotemia was associated with elevated lactic dehydrogenase (LDH) and uric acid levels, and sometimes extrinsic ureteral obstruction by tumor. Two patients required dialysis for uric acid nephropathy before chemotherapy was initiated. Following chemotherapy, major complications of tumor lysis (hyperuricemia, hyperkalemia and hyperphosphatemia) were associated with very large tumors, high LDH levels and inadequate urinary output. In patients undergoing diuresis and receiving allopurinol, hyperkalemia or hyperuricemia developed infrequently unless concomitant renal failure ensued. Hyperphosphatemia, which occurred only after chemotherapy, developed in 10 of 32 (31 per cent) nonazotemic and in all azotemic patients. Hemodialysis was required in three post-treatment patients for control of azotemia, hyperuricemia, hyperphosphatemia and/or hyperkalemia. Because of the potential for renal failure caused by precipitation of phosphate, severe hyperphosphatemia is an additional criterion for dialysis in patients with acute tumor lysis syndrome.

Adolescent↗

PubMed1989

Dosing of contrast material to prevent contrast nephropathy in patients with renal disease.

PURPOSE: Contrast-induced renal dysfunction has been reported to occur in 15% to 42% of patients with underlying azotemia, but there is disagreement as to whether its incidence is reduced by limiting the amount of contrast material. To adjust the amount of contrast material to the severity of azotemia, we have utilized the following formula to calculate a contrast material "limit" in patients with renal disease: Contrast material limit = (formula; see text) PATIENTS AND METHODS: Over a 10-year period, 115 patients (53 men, 62 women, aged 61 +/- 11 [mean +/- SD] years) with renal dysfunction (baseline serum creatinine level greater than or equal to 1.8 mg/dL) underwent cardiac catheterization and angiography, after which the level of serum creatinine was measured daily for five days. The amount of contrast material that was given adhered to the limit in 86 patients (Group I) and exceeded it in 29 (Group II). RESULTS: Contrast-induced renal dysfunction (an increase in serum creatinine greater than or equal to 1.0 mg/dL) occurred in two (2%) patients in Group I and in six (21%) patients in Group II (p less than 0.001). Of the 48 patients with concomitant diabetes mellitus, the contrast limit was surpassed in 16, six (38%) of whom had contrast nephropathy. Only two of the 32 (6%) diabetic patients in whom the contrast limit was not exceeded had contrast nephropathy (p less than 0.001). CONCLUSIONS: Thus, contrast-induced renal dysfunction occurs infrequently if the amount of contrast material is limited in accordance with the degree of azotemia. Diabetic patients have a high incidence of contrast nephropathy, particularly when they receive an excessive amount of contrast. In patients with diabetes and renal impairment, it may be preferable to perform angiography as a staged procedure or to utilize alternative (non-contrast) techniques to obtain the desired information rather than to exceed the prescribed contrast limit.

Acute Kidney Injury↗

PubMed1995

Interventions in clinical acute renal failure: what are the data?

A variety of therapeutic approaches have been used both to prevent acute ischemic and nephrotoxic renal injury and to improve renal function and reduce mortality once acute renal failure (ARF) has developed. Unfortunately, there have been few rigorous assessments of the efficacy of these treatment interventions. The reasons for the lack of abundant critical data regarding treatment effects in ARF are several. First, ARF is a functional disorder. It has a spectrum of etiologies, occurs in a variety of clinical settings and varies in severity. Second, selected endpoints of treatment success vary and co-morbid factors frequently determine outcome. Third, it had been difficult to carry out prospective controlled studies in a disorder in which the mortality rate approaches 50%. In this review, an effort was made to analyze the available literature with a primary focus on controlled studies to determine significant prophylactic and treatment effects of various interventions in ARF. Three endpoints of therapy (change in renal function, change in course of azotemia, and change in mortality) were examined for pharmacologic agents. Changes in course of azotemia and mortality were assessed in evaluating different dialysis modes. Effect on nitrogen balance, change in course of azotemia, and change in mortality were used as endpoints to determine treatment effects of different nutritional regimens. When weight was given to prospective controlled studies, some insights emerged as to treatment interventions that are most likely to have beneficial effects in specific settings of ARF. Among pharmacologic agents, mannitol appears to have a positive prophylactic effect in kidney transplantation. There are no other significant beneficial effects of diuretics for prophylaxis or as treatment in early or established ARF. Of vasoactive agents, there is a relatively small amount of data suggesting that diltiazem may have a positive prophylactic effect in kidney transplantation, and dopamine possibly is beneficial early in the evolutionary phase of ARF. Atrial natriuretic peptide and calcium channel blockers may have beneficial effects in established disease. No other pharmacologic interventions are supported by substantial data. At best, the results are equivocal regarding the use of early and vigorous dialysis in ARF. However, there are recent impressive data indicating that the use of biocompatible membranes is efficacious in recovery and survival. There is no clear evidence that one form of nutritional therapy has advantages over others, but some level of amino acid supplementation in addition to basic energy replacement is supported by the overall data.

Acute Kidney Injury↗

PubMed1996

An immunocytochemical study of H+ ATPase in kidney transplant rejection.

Kidney transplant rejection may be accompanied by defective urinary acidification. Its pathogenesis is unknown. There are shared histologic features between kidney transplant rejection and the distal renal tubular acidosis (RTA) of Sjogren syndrome, which led us to hypothesize that deficient collecting duct H+ adenosine triphosphatase (ATPase) expression--which is lacking in the RTA of Sjogren syndrome - may cause the RTA of kidney transplant rejection. Six kidney transplant recipients with biopsy evidence for rejection and two control subjects were studied physiologically and by immunohistochemistry. We found defective urinary acidification in all 6 kidney transplant patients. Ammonium excretion was diminished in relation to the degree of azotemia. There was an abnormal response to furosemide in all 6, suggesting distal tubular dysfunction. Distal H+ ATPase staining was reduced in relation to the degree of azotemia, although it was not totally absent even in the worst case. This was paralleled by the urinary PCO2 response. Both control subjects had good urine PCO2 and H+ ATPase staining and adequate urine pH response to furosemide. They had reduced urinary ammonium (NH4) concentrations in relation to modest azotemia. We conclude that kidney transplant rejection may be accompanied by defective urinary acidification, which is not primarily due to a lack of H+ ATPase. The RTA of kidney transplant rejection appears to result from defective ammonium excretion, generalized distal tubular malfunction, and--in severe cases--from a reduction in distal nephron H+ ATPase expression.

Acidosis, Renal Tubular↗

PubMed1999

Angiotensin II infusion exacerbates radiation nephropathy.

We hypothesized that angiotensin II will exacerbate radiation nephropathy in a time-specific manner. Experimental radiation nephropathy is treatable with angiotensin-converting enzyme inhibition or angiotensin II (AII) receptor blockers. These interventions are particularly important between 3 and 10 weeks after irradiation. We therefore undertook studies in which AII infusions were given at particular intervals after irradiation. Rats received total body irradiation (TBI) plus syngeneic bone marrow transplantation followed (or not) by AII infusion at 200 or 400 ng/kg/min. Infusions were given from 0 to 4 or 4 to 8 weeks after irradiation. An additional group was unirradiated but infused at 800 ng/kg/min for 8 weeks. Kidney function was assessed over 26 weeks, and histology was evaluated after the animals were killed. AII infusion alone did not cause azotemia. There was transient hypertension during AII infusion at 800 ng/kg/min but only minor histologic injury. Irradiation caused azotemia and hypertension, which were not exacerbated by AII infusion at 200 ng/kg/min. Irradiation plus AII infusion at 400 ng/kg/min from 4 to 8 weeks after TBI caused significantly greater azotemia than irradiation alone or irradiation with AII infusion from 0 to 4 weeks. The blood pressure was higher in irradiated rats infused with AII from 4 to 8 weeks. Arteriolar fibrinoid necrosis was a prominent feature in kidneys of rats infused with AII from 4 to 8 weeks after TBI. The worsening of radiation nephropathy by AII infusion from 4 to 8 weeks after irradiation strongly supports the idea of specific and sequential events in the pathogenesis of kidney failure in this model. Hypertension may play a role in these events in addition to the effect of AII alone. The occurrence of arteriolar fibrinoid necrosis in the irradiated, 4-to-8-week-infused animals suggests that vascular injury during that interval determines later outcome.

Angiotensin II↗

PubMed1979

Upper tract management when posterior urethral valve ablation is insufficient.

Of 105 boys with posterior urethral valves managed during a 10-year period most were managed by primary valve ablation. However, 39 of these boys required concomitant or additional procedures to 71 massively dilated ureters because of azotemia, infection and/or progressive upper tract deterioration. In 17 boys 25 ureters could be reconstructed primarily by varying degrees of ureteral tailoring. When there was severe infection, azotemia and/or doubt as to the function of the affected renal unit, staged reconstruction was initiated by cutaneous ureterostomy. One-fourth of these ureterostomy diverted children died of azotemia despite free urinary drainage. Those who went on to have staged reconstruction, despite multiple surgical procedures, retained intact urinary systems with acceptable function.

Bacterial Infections↗

PubMed1997

Gender and the effect of gonadal hormones on the progression of inherited polycystic kidney disease in rats.

Human autosomal dominant polycystic kidney disease (ADPKD) is a common inherited disease and displays a gender dimorphism in renal disease progression. Han:SPRD-Cy rats manifest a form of ADPKD that is similar in many respects to that seen in humans. In Han:SPRD rats, male Cy/+ rats have more prominent renal changes and develop renal failure at an early age, whereas female Cy/+ rats exhibit less severe renal cystic change and have normal renal function until advanced age. To determine whether the male gonadal hormone, testosterone, contributes to this gender dimorphism, males were sham operated or castrated; some castrated rats were repleted with 5alpha-dihydrotestosterone. Female rats were sham operated or ovariectomized before sham operation or testosterone treatment. All treatments started at 4 weeks of age and ended at 10 weeks of age. Renal enlargement, cystic change, and renal function were assessed. In the males, castration reduced renal enlargement and cystic change; testosterone treatment abrogated these effects. Neither of these manipulations affected azotemia in male Cy/+ rats. In the females, testosterone was renotropic for both normal and cystic kidneys. In the Cy/+ females, testosterone treatment caused azotemia and an increase in the severity of the PKD. Ovariectomy blunted the effect of testosterone on cystic kidney enlargement. Testosterone treatment did not completely erase the gender-associated differences in azotemia in the Cy/+ rat. These data confirm the renotropic effects of testosterone and indicate that testosterone influences the progression of renal cystic change in male and female rats with ADPKD.

Animals↗