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PubMed1989

Atrial natriuretic peptide in patients with obstructive uropathy.

Renal response to release of bilateral ureteral obstruction resembles that to intravenous administration of atrial natriuretic peptide. In a prospective study we measured plasma atrial natriuretic peptide levels before and serially after relief of obstruction in 9 patients (mean age 65 +/- 2 years old) with bilateral ureteral obstruction and azotemia. Obstruction was documented by renal ultrasonography. Before relief of obstruction blood urea nitrogen and serum creatinine levels were 85 +/- 18 (mean +/- standard error) and 8.2 +/- 1.3 mg. per dl., respectively, accompanied by metabolic acidosis but not hyperkalemia. Mean plasma atrial natriuretic peptide (measured by radioimmunoassay) was 129 +/- 28, which was markedly elevated compared to 46 +/- 7 pg. per ml. in 7 age-matched control subjects (p less than 0.01). After relief of obstruction, prominent post-obstructive diuresis and natriuresis ensued; the plasma atrial natriuretic peptide level progressively decreased to that noted in the control group, accompanied by improvement in renal function, and diminishing diuresis and natriuresis. These findings were associated with a significant weight loss and an increase in plasma renin activity (from a mean of 1.57 +/- 0.68 to 5.27 +/- 1.82 ng. per ml. per hour, p less than 0.01). These results suggest that atrial natriuretic peptide release is augmented in patients with bilateral ureteral obstruction and azotemia, probably due to hypervolemia, and may contribute to post-obstructive diuresis and natriuresis.

Atrial Natriuretic Factor↗
PubMed1991

Community-acquired acute renal failure.

Acute renal failure usually occurs during hospitalization, but may also be present on admission to the hospital. To define the causes and outcomes of community-acquired acute renal failure, we undertook a prospective study of patients admitted to the hospital with acute elevations in serum creatinine concentrations. Over a 17-month period, all admission serum creatinine determinations were screened for patients with values greater than 177 mumol/L (2 mg/dL). These values were compared with baseline creatinines to select patients with an acute elevation in serum creatinine occurring outside the hospital. One hundred patients were entered into the study, with an overall incidence of 1% of hospital admissions. Seventy percent of the patients had prerenal azotemia, 11% had intrinsic acute renal failure, 17% had obstruction, and 2% could not be classified. Mean peak serum creatinine (318 +/- 18 mumol/L [3.6 +/- 0.2 mg/dL]) and mortality (7%) was lowest in the group with prerenal azotemia. In this group, volume contraction due to vomiting, decreased fluid intake, diarrhea, fever, glucosuria, or diuretics was the most common underlying cause. The group with intrinsic acute renal failure had the most severe renal failure and the highest mortality (55%). Although ischemic acute tubular necrosis is the most common cause of hospital-acquired intrinsic acute renal failure, this etiology was seen in only one patient. Drug-induced nephrotoxicity and infection-related causes were the most common underlying etiologies of intrinsic acute renal failure. Obstructive renal failure had a mortality of 24% and was most commonly due to benign prostatic hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1986

gamma-Glutamyl transpeptidase excretion in cisplatin-induced acute renal failure.

Cisplatin (cisdiamminedichloroplatinum), an important antineoplastic agent, possesses nephrotoxicity as its major side effect. A mild partially reversible nonoliguric form of acute renal failure (ARF) is generally the most common form of nephrotoxicity and occurs in experimental animals following a single dose. gamma-Glutamyl transpeptidase (gamma GT) is an enzyme with maximal activity located in the brush border of proximal renal tubular epithelium. To test the relationship between cisplatin nephrotoxicity and urinary gamma GT excretion, rats received a single 5.5 mg/kg dose of cisplatin and gamma GT excretion was evaluated and compared to anatomic and functional damage. Twenty-four hours following cisplatin administration, there was a marked enhancement of urinary gamma GT excretion, prior to the onset of azotemia. Urinary gamma GT excretion peaked at day 4, then returned to baseline, and decreased to values below baseline on days 8 through 10. By days 11 through 12, renal function and urinary gamma GT excretion had returned to normal. The correlation between nephrotoxicity, changes in urinary gamma GT excretion, and anatomic damage was excellent. Morphologically, increased gamma GT excretion was associated with loss of microvilli, and the return of urinary gamma GT excretion to normal correlated with their regeneration. We conclude that cisplatin administration results in increased urinary gamma GT excretion. This early enhancement, prior to the onset of azotemia, may provide a useful noninvasive marker of early cisplatin nephrotoxicity.

Acute Kidney Injury↗
PubMed1988

Urinary doubly refractile lipid bodies in nonglomerular renal diseases.

Urinary doubly refractile lipid bodies (DRLB) are a characteristic finding in patients with glomerular renal diseases causing heavy proteinuria. DRLB are felt to be an uncommon finding in glomerular diseases without heavy proteinuria, and a rare finding in nonglomerular renal diseases. In order to determine whether DRLB are found in nonglomerular renal diseases, we reviewed the medical records of all patients who had urinalyses performed in our laboratory from February 1975 to June 1983. Three hundred sixty one patients demonstrated less than or equal to +2 proteinuria, and at least two DRLB. Of these, 290 were identified as having a single renal diagnosis. One hundred forty eight patients (51%) had a variety of acute and chronic glomerular diseases, and 125 patients (43.2%) had nonglomerular renal diseases, including acute tubular necrosis (ATN), prerenal azotemia, chronic interstitial nephritis, polycystic kidney disease, acute interstitial nephritis, renal neoplasia, and acute myeloma kidney. Ten patients had transient proteinuria associated with acute illness, and seven patients had no renal disease at all. Only two patients with nonglomerular renal disease had more than five DRLB per 20 high power microscopic fields. The frequency of DRLB in patients with nonglomerular renal diseases was: chronic interstitial nephritis, 26%; polycystic kidney disease, 38%; prerenal azotemia, 20%; ATN, 15%; and acute interstitial nephritis, 33%. These data suggest that at lower levels of proteinuria, DRLB are found frequently in nonglomerular renal diseases, and that DRLB do not differentiate glomerular from nonglomerular renal diseases unless more than five DRLB are found on urinary sediment examination.

Humans↗
PubMed1997

The effect of paclitaxel on the progression of polycystic kidney disease in rodents.

Woo et al (Nature 368:750-753) reported that parenteral administration of paclitaxel arrested the striking renal enlargement and prolonged life in C57BL/6J-cpk/cpk mice with a rapidly progressive form of polycystic kidney disease (PKD). In the current study, we sought to determine whether paclitaxel could alter the progression of other forms of hereditary PKD in rodents. Paclitaxel was administered by intraperitoneal injection to C57BL/6J-cpk/cpk mice and Han:SPRD-Cy/Cy rats with rapidly progressive PKD and to DBA/2FG-pcy/pcy mice and Han:SPRD-Cy/+ rats with slowly progressive PKD. Paclitaxel (150 micrograms/wk) prolonged the survival of cpk/cpk mice from 24.5 days to more than 65 days and decreased kidney weight relative to body weight from 16.5% at 21 days of age to 8.2% at more than 65 days of age. Mortality attributable to paclitaxel was 12%. By contrast, the administration of paclitaxel (0.1 to 15 mg/kg/wk) to 7- to 10-day-old Han:SPRD-Cy/Cy rats with rapidly progressive PKD had no effect on the course of the disease; moreover, paclitaxel caused severe side effects and premature death in all the Cy/Cy animals. Heterozygous male Cy/+ rats develop slowly progressive renal enlargement and azotemia. Paclitaxel, administered at 7, 15, or 27 mg/kg/wk to male Cy/+ rats from 4 until 10 weeks of age, reduced body weight gain, had an inconsistent effect on kidney weight relative to body weight, and had no effect on the serum urea nitrogen concentration. Mortality associated with the 7, 15, and 27 mg/kg/wk doses of paclitaxel was 0%, 15.4%, and 28.5%, respectively. DBA/2FG-pcy/pcy mice of either sex developed slowly progressive renal enlargement and azotemia. The administration of paclitaxel (100 to 150 micrograms/wk) from 2 to 10 weeks of age to DBA/2FG-pcy/pcy mice with cystic disease had no effect on the increase in kidney weight or on the level of serum urea nitrogen in comparison to untreated cystic animals. Mortality associated with 100- and 150-micrograms/wk doses of paclitaxel was 0% and 20%, respectively. We conclude that paclitaxel diminished the rate of renal enlargement and increased the life span of cpk/cpk mice but not Cy/Cy rats with rapidly progressive forms of PKD. Paclitaxel had no apparent benefit in Cy/+ rats nor pcy/pcy mice with slowly progressive PKD. On the basis of these studies in rodents, it appears that paclitaxel has limited potential usefulness as a therapeutic agent in the treatment of PKD.

Animals↗
PubMedDate not supplied

Hepatorenal syndrome: a disease mediated by the intrarenal action of renin.

The functional renal failure accompanying advanced liver disease is characterized by azotemia, a urine of very low sodium concentration and systemic hypotension with decreased renal perfusion and high renal vascular resistance. Patients with this disorder have a markedly reduced ability to excrete free water and develop hyponatremia, ascites and edema. It is postulated that this renal dysfunction is due to hepatic failure to make renin substrate. Renin released from the kidney is thus unable to exert its pressor effect. The resultant hypotension and renal hypoperfusion continue to stimulate excessive synthesis and release of renin. It is postulated that the overdriven renal renin system increases renovascular resistance at the level of the glomerular arterioles. This causes decreased renal blood flow and decreased glomerular filtration rate leading to salt and water retention and azotemia. Since no renin substrate is available for human infusion, this hypothesis could be tested either by infusion of angiotensin II to restore systemic blood pressure and renal perfusion or by beta adrenergic blockade with propranolol to attempt to decrease the intrarenal effects of renin, restore glomerular blood flow and filtration and thus return of renal function.

Angiotensin II↗
PubMed1995

The effects of food and drink on the survival of binephrectomized rats.

Previous studies have shown that the survival time of rats following binephrectomy is between 48 and 120 hours. The aim of the present study was to examine the assumption that the eating and drinking protocol before and after binephrectomy affects the survival time following surgery in male, female and young rats. In this study we used protocols which included various combinations of eating and drinking or their prevention before and after binephrectomy. Survival time was determined by examining the kinetics of death following binephrectomy. Examination of the azotemia and physiological condition of the rat was performed by testing BUN, creatinine, plasma Na and K concentrations as well as the hematocrit. All rats that had eaten and drunk before and after binephrectomy, in various combinations, died within 48 hours. Rats that did not eat or drink before and after binephrectomy died within 72 hours (p < 0.001). Rats that did not eat before and after the binephrectomy but had free access to drink died within 90 hours of the surgery (p < 0.001). From this study it can be concluded that the eating and drinking protocol before and after binephrectomy affects the survival time of male, female and young rats. The effect varies between a survival time of 48 and 90 hours following binephrectomy. A possible explanation for this effect is that the eating and drinking protocol affects the rate of azotemia formation.

Animals↗
PubMed1983

Amelioration of experimental glomerulonephritis by dietary protein restriction.

We have examined the effects of various levels of dietary protein intake on the course of nephrotoxic serum nephritis in the rat by feeding low (4.6% casein), standard (23% casein), and high (57.5% casein) protein diets which were identical in calorie, mineral, and electrolyte content. Nephritic rats on a high protein diet manifested heavy proteinuria, hypoalbuminemia, hypercholesterolemia, azotemia, and elevated serum creatinine levels. In those subjected to dietary protein restriction, proteinuria remitted and azotemia did not develop. While mesangial widening, interstitial abnormalities, and segmental proliferation and sclerosis of glomeruli occurred regularly in nephritic rats fed high protein diets, histologic abnormalities were virtually absent in those on low protein intake. Animals on a standard protein intake manifested histologic and clinical features intermediate in severity. We conclude that the renal functional and histologic consequences of nephrotoxic serum nephritis can be averted by dietary protein restriction.

Animals↗
PubMed1994

Post-ischemic acute renal failure protects proximal tubules from O2 deprivation injury, possibly by inducing uremia.

Rats within the early maintenance phase of post-ischemic acute renal failure (ARF) can resist additional ischemic insults. This study assessed whether this protection exists directly at the tubular cell level, and if so, whether it is a consequence of prior cell injury (for example, due to heat-shock protein synthesis; HSP), or if it arises in response to reductions in functional renal mass and/or the uremic environment. Rats were subjected to either 15 or 35 minutes of unilateral or bilateral renal ischemia, and after 15 minutes to 24 hours of reflow, proximal tubular segments (PTS) were isolated for study. Their viability following oxygenation and hypoxic/reoxygenation injury (H/R) was tested (LDH release). The influence of uremia/reduced renal mass was determined by studying PTS extracted 24 hours after 1 1/2 nephrectomy, and by determining whether PTS exposure to a "uremic milieu" (urine addition) blocks H/R damage. HSP effects were gauged by correlating renal cortical HSP-70 expression with degrees of in vitro protection, and by ascertaining whether in vivo hyperthermia (42 degrees C; 15 min) mitigates subsequent PTS H/R damage. Results were compared with those obtained from normal PTS. The in vivo experimental protocols did not substantially alter PTS isolation or their viability during oxygenation. Fifteen minutes of ischemia induced neither azotemia nor PTS cytoprotection. In contrast, 35 minutes of ischemia conferred marked protection against subsequent H/R, but only when azotemia was permitted to develop (protection seen after 24 hr, but not at 4 hr of reflow; protection abrogated by retention of 1 normal kidney). Renal failure in the absence of tubular necrosis (1 1/2 uninephrectomy) protected PTS from H/R damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed2003

Mycophenolate mofetil in pediatric liver transplant patients with renal dysfunction: preliminary data.

The prolonged use of CNI has been associated with nephrotoxicity. MMF is a new immunosuppressive agent. In the present study, the consequences of introducing MMF and reduction of CNI in liver-transplant children were analysed. The present study included eight pediatric liver-transplant patients who had transplantation at least 5 yr previously, had stable graft function and had renal dysfunction as a probable side-effect of CNI therapy. CNI was replaced with MMF in all patients and serum creatinine, uric acid concentration, azotemia and creatinine clearance before and 6 months after study entry were measured. The patients were monitored closely for side-effects of MMF as well as graft function. Six months after study entry serum creatinine, uric acid concentration, azotemia and creatinine clearance improved in all the patients at the last follow-up. The aspartate aminotransferase and alanine aminotransferase concentrations were stable during the study period and did not observe any serum bilirubin increased as well. No side-effects were reported in patients on MMF. Only one patient reported temporary pruritus and nausea. The results indicate that renal dysfunction significantly improved when MMF therapy is started and CNI reduced. Furthermore present data suggest that the risk of acute allograft rejection is very low when the CNI desired reduction is achieved in not too short time and absolutely when the MPA levels are strictly monitored.

Acute Kidney Injury↗
PubMed1984

Renal revascularization in the azotemic hypertensive patient resistant to therapy.

We undertook this study to assess the frequency of renovascular hypertension in patients with azotemia and hypertension refractory to drug therapy and to determine the effects of renal revascularization on blood pressure and renal function in these subjects. Thirty-nine of 106 consecutive patients admitted for diagnostic evaluation of severe hypertension proved to have renovascular hypertension. Of 21 hypertensive patients with renal insufficiency, 10 appeared to have renovascular hypertension with either bilateral atherosclerotic renovascular disease or unilateral renal arterial stenosis in a solitary functioning kidney. Medical therapy in the hospital often induced further deterioration of renal function despite enhanced blood-pressure control. However, surgical revascularization or percutaneous transluminal angioplasty produced improvement or stabilization of renal function and control of blood pressure in all patients with azotemia who were treated in this manner, despite longstanding hypertension. The benefits of therapy have persisted for 10 to 42 months of follow-up. These studies indicate that refractory hypertension in association with renal insufficiency is a relatively common clinical presentation for renovascular hypertension and bilateral renal-artery disease. Diagnostic evaluation and consideration of renal revascularization appear warranted in such patients, both for the control of the hypertension and for improvement in renal function.

Aged↗
PubMed2002

The renin-angiotensin system in experimental radiation nephropathy.

Irradiation of the kidneys is followed by a well-defined sequence of changes leading eventually to kidney failure. In the rat, inhibition of angiotensin-converting enzyme or blockade of angiotensin II receptors can prevent the structural and functional changes that occur after kidney irradiation. These interventions are particularly effective between 3 and 10 weeks after irradiation. However, in a series of studies with the rat model we failed to find any evidence that the renin-angiotensin system (RAS) is activated in the first 10 weeks after kidney irradiation. First, if the RAS was activated during this interval, one would expect hypertension followed by proteinuria and azotemia. However, hypertension is significant only at the end of this period and is preceded by significant proteinuria and azotemia. This evolution is not in favor of an obviously activated RAS during the 3- to 10-week postirradiation interval that is critical for interventions aimed at the RAS. Second, plasma renin activity and active plasma renin protein concentrations are not significantly increased over the first 10 weeks after irradiation. Third, whole-blood and intrarenal angiotensin II levels are not increased and may even be decreased over this interval. This last observation is particularly important because the assay used is sensitive enough to detect the effects of dietary salt manipulation. We hypothesize that even the normal activity of the RAS contributes to injury after kidney irradiation, possibly by supporting the proliferation of cells that carry potentially lethal radiation injuries.

Animals↗
PubMed2001

An enormous abdominal mass associated with acute renal failure.

We report a 67-year-old man with acute uric acid nephropathy, secondary to spontaneous tumor lysis syndrome, that presented itself as a huge intra-abdominal tumor that led to acute renal failure, hyperuricemia, and azotemia. Initial finding of hydronephrosis detected by ultrasonography led us to believe that the azotemia and decreasing amount of urine resulted from obstructive uropathy, a common complication of malignancy, caused by either a direct renal invasion or a urinary outflow tract compression because of a tumor mass effect. However, clinical observations and the response to therapeutic intervention confirmed the diagnosis of spontaneous tumor lysis syndrome, which is a rare cause of acute uric acid nephropathy.

Abdominal Neoplasms↗
PubMed1962

Glomerulonephritis induced in sheep by injections of heterologous glomerular basement membrane and Freund's complete adjuvant.

Sheep injected every 2 weeks with heterologous GBM and Freund's adjuvant by any one or combination of the following routes: intramuscular, subcutaneous, or intradermal, develop uniformly a fulminating, extracapillary glomerulonephritis, invariably fatal within 27 to 90 days after the first injection. The chief histologic feature is marked fibroepithelial proliferation of Bowman's capsule with crescent formation. The appearance of the lesions resembles the acute, subacute, and chronic stages of human glomerulonephritis, and depends on when the animal was sacrificed. Freund's adjuvant or heterologous GBM alone does not produce such a nephritis. The combination of placental tissue and Freund's adjuvant under the present experimental conditions was also unable to produce a nephritis. The clinical course, increase in nitrogen retention, evolution of renal lesions, and death, all describe a fulminating disease. The disease most characteristically resembles fatal, fulminating human subacute glomerulonephritis. The changes in serum proteins, decrease in serum albumin, and increase in serum globulin, occurred approximately the same in both the GBM-treated and the control adjuvant group. Similar changes have been reported from hyperimmunization alone, and so it is not clear how much these changes are due to immunization and how much is due to the nephritic process. The changes in serum cholesterol were not considered statistically significant. Circulating serum antibodies which localized (by fluorescent antibody technique in vitro) on basement membrane structures of the heterologous donor kidney antigen or which produced nephritis in the heterologous donor species (rat and dog) were found in serum of sheep sick or dying of nephritis. The passive transfer of nephritis by serum antibodies marks the first successful instance of transfer of nephritis by serum antibody to a heterologous species from an animal which had developed nephritis itself. The serum antibodies involved in the transfer of disease to the donor species appear to be unrelated to the mediators of nephritis in the sheep and may represent only the previously known heteronephrotoxic antibodies. By various biologic criteria the sheep nephritis presumably occurs by an autoimmune mechanism. However, it is not known whether the sheep nephritis is mediated by sensitized cells and/or antibodies. The latent period was estimated to end about 16 to 71 days after the first injection. Azotemia was estimated to begin about 17 to 78 days after the first injection. Proteinuria and azotemia began approximately 23 and 13 days before death. The rapid progression to a fatal termination defined the fulminating character of this disease.

Animals↗
PubMed1990

Energy metabolism in acute and chronic renal failure.

Energy metabolism was measured by indirect calorimetry in 86 patients with various forms of renal failure and in 24 control subjects. In patients with acute renal failure with sepsis, oxygen consumption, carbon dioxide production, and resting energy expenditure were increased (P less than 0.05). In other groups with renal failure (acute renal failure without sepsis, chronic renal failure with conservative treatment or hemodialysis, and severe untreated azotemia) these indices were not different from those of control subjects. Urea nitrogen appearance was decreased in patients with chronic renal failure undergoing conservative treatment, in those with severe untreated azotemia, and in hemodialysis patients (P less than 0.05). We conclude that renal failure has no influence on energy expenditure as long as septicemia is absent. Reduced urea nitrogen appearance rates in chronic renal failure are due to a reduced energy and protein intake. Wasting is a consequence of decreased food intake but not of hypermetabolism in chronic renal failure.

Acute Kidney Injury↗
PubMed1990

Tumor lysis syndrome after induction chemotherapy in small-cell lung carcinoma.

Small-cell lung cancer (SCLC) is responsive to combination chemotherapy. Response rates of 50-80% can be achieved depending on whether the cancer is limited or extensive. Rarely, patients with SCLC respond so rapidly to induction chemotherapy that they develop a tumor lysis syndrome. This syndrome may lead to azotemia and renal failure if not recognized early and treated appropriately. This complication of therapy is important to recognize as the treatment of SCLC is sometimes administered on an outpatient basis. In addition, certain chemotherapeutic agents used in SCLC, such as cis-platin, are nephrotoxic and could potentially aggravate the azotemia secondary to the tumor lysis syndrome.

Acute Kidney Injury↗
PubMed2000

Acute renal failure in HIV-infected patients: a brief review of common causes.

Acute renal failure is a well-described renal syndrome observed in patients infected with the human immunodeficiency virus (HIV). Underlying glomerular disease and disturbances in renal tubular function predispose these patients to a number of hemodynamic and nephrotoxic insults. Prerenal azotemia from both "true" and "effective" depletion of intravascular volume is the most common cause of acute renal insufficiency in patients infected with HIV. Direct damage to the renal tubules from both nephrotoxic medications and prolonged ischemic processes occurs frequently in hospitalized patients. Injury to the tubulointerstitium of the kidney may also result from allergic reactions to medications prescribed to patients. Deposition of crystals in the tubular lumens, and rarely in the glomerular capillaries, will cause acute renal failure in the setting of tumor lysis syndrome or during therapy with medications associated with crystal nephropathy. Finally, obstruction of the urinary system will rarely cause postrenal azotemia in patients infected with HIV.

Acute Kidney Injury↗
PubMed1984

Aortic and renal vascular disease. Factors affecting the value of combined procedures.

Assessment of the predictive value of preoperative factors in the determination of operative risk in 50 patients who underwent simultaneous aortic and renovascular procedures over a 10-year period is reported. There were six operative mortalities (12%). Factors associated with increased mortal risk were azotemia (43% vs. 7%), associated complex renal or visceral procedures (31% vs. 5%), treatment of aortic aneurysm vs. occlusive disease (17% vs. 5%), positive EKG (19% vs. 4%), age over 60 years (20% vs. 4%), and a history of diffuse peripheral vascular disease (18% vs. 7%). None of these differences, by themselves, had statistical significance. Through discriminate analysis with assignment of weighted scores to the five most powerful predictors of operative death (complex procedure--4, azotemia--4, aortic aneurysm repair--3, positive electrocardiogram--2, history of diffuse vascular disease--2), a weighted score of greater than or equal to 10 predicted operative death with an 83% sensitivity and 93% specificity (p = 0.003). Although advanced age, diabetes, severity of hypertension, and history of heart disease were associated with increased operative risk, they contributed minimal discriminate value to that provided by the preceding five variables. This was because these weaker risk factors were usually found in association with the predictors in the discriminant score. This study suggests that in patients with high weighted discriminant scores (greater than or equal to 10), consideration of operative risk is particularly important in evaluation of the proposed value of combined procedures.

Adult↗