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PubMed1998

Serum creatinine and blood urea nitrogen over a six-year period in the very old. Creatinine and BUN in the very old.

In a population of 141 very elderly subjects, there was a small but significant decline in BUN and creatinine at 3 years, which persisted at 6 years although partially attenuated. A similar pattern of falling BUN and creatinine was seen in the 31 subjects who began the study with mild azotemia. There was no significant change in the subjects' mean Body Mass Index during the 6-year period of observation. The azotemic subjects had a rate of death or dropout from the study similar to that of the entire cohort. Mean systolic blood pressure fell by 5.4 mm Hg (p < 0.05) and diastolic blood pressure by 2.1 mm Hg (p = NS) by 6 years. Users of diuretics or NSAID had a mean BUN and creatinine comparable to those not taking these medications. We conclude that BUN and serum creatinine do not necessarily increase with time in the old old, even in those with mild azotemia, hence, several determinations of these parameters may be needed to ensure accuracy. While renal function in the elderly probably does not improve with time, it may stabilize due to improvement in blood pressure. Use of diuretics and NSAID by functioning elderly individuals is not necessarily associated with worsening azotemia.

Aged↗
PubMed1993

Autosomal-dominant polycystic kidney disease in the rat.

Kaspareit-Rittinghausen described a rodent model of inherited polycystic kidney disease (PKD), the Han:SPRD rat [1, 2], in which heterozygotes develop renal cysts and renal failure (in males) over several months, whereas homozygous animals develop rapidly progressive renal enlargement that leads to death in a few weeks. In this study, we examined selected elements of the pathogenesis of this disease in heterozygotes and homozygotes from birth to advanced disease. Heterozygous male rats developed slowly progressive renal cystic disease with interstitial fibrosis and azotemia seen by six months of age. Female heterozygotes developed slowly progressive renal cystic disease, but did not develop interstitial fibrosis or azotemia. Epithelial cells lining cyst cavities showed various degrees of morphologic immaturity. Cyst walls also developed basement membrane thickening, especially in areas of cellular immaturity, suggesting an interrelationship between this basement membrane thickening and cellular dedifferentiation. Thickened basement membranes were associated with increased immunoreactivity for type IV collagen, laminin, and fibronectin. Homozygous rats developed massive renal enlargement, marked azotemia, and died near three weeks of age. Renal c-myc proto-oncogene expression was elevated in homozygous cystic infants and in adult heterozygotes. In situ hybridization showed high levels of c-myc mRNA in cyst epithelia, suggesting abnormal regulation of cellular proliferation in the cells lining cysts, as seen in other models of PKD. The Han:SPRD rat is the only well-documented animal model of inherited PKD with an autosomal-dominant inheritance pattern and appears to have several features which resemble human ADPKD.

Animals↗
PubMed1997

Noncontinuous use of angiotensin converting enzyme inhibitors in the treatment of experimental bone marrow transplant nephropathy.

Angiotensin-converting enzyme (ACE) inhibitors can be used to prevent the development of radiation nephropathy after BMT. In previous BMT nephropathy studies, ACE inhibitor therapy was started pre-BMT and continued indefinitely. In preparation for clinical trials, studies were designed to determine whether effective prophylaxis could be achieved if ACE inhibitor therapy was started after engraftment, and to determine whether ACE inhibitors needed to be given indefinitely. The present studies in our rat syngeneic BMT model showed that captopril therapy started 25 days post-BMT was as effective as therapy started prior to BMT. When ACE inhibitor therapy was discontinued 28 weeks after BMT, the protective effect was not lost if adequate control of azotemia had been maintained for 26 weeks. If adequate control of azotemia was not maintained for 26 weeks, BMT nephropathy progressed rapidly when ACE inhibitor therapy ended, and slowly when it was continued. Failure to control azotemia was a better predictor of renal failure than failure to control hypertension or proteinuria. Based on these preclinical studies, it would appear that ACE inhibitor therapy will be effective in the prophylaxis of BMT nephropathy even if begun after engraftment, and that ACE inhibitors may not need to be given indefinitely.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Cohort study of the treatment of severe HIV-associated nephropathy with corticosteroids.

BACKGROUND: Human immunodeficiency virus-associated nephropathy (HIVAN) results in rapidly progressive azotemia. The effectiveness and safety of corticosteroids in the treatment of HIVAN, however, remains controversial. METHODS: We conducted a retrospective cohort study of patients with biopsy-proven HIVAN and progressive azotemia who were eligible for corticosteroid treatment and who had no clinical or histologic evidence of an alternative cause of acute renal failure. Selected patients were treated with 60 mg of prednisone for one month, followed by a several-month taper. RESULTS: Twenty-one eligible patients were identified. Thirteen subjects had received corticosteroid treatment, whereas eight had not. The mean serum creatinine was 6.2 and 6.8 mg/dL, respectively (P > 0.05). The relative risk (95% CI) for progressive azotemia with corticosteroid treatment at three months was 0.20 (0.05, 0.76, P < 0.05). This association remained significant despite adjustment in separate logistical regression analyses for baseline creatinine, 24-hour proteinuria, CD4 count, history of intravenous drug use, hepatitis B, and hepatitis C. In an additional logistic regression model, using backward stepwise selection of the previously mentioned covariates, only corticosteroid treatment (P = 0.02) and baseline serum creatinine (P = 0.10) were retained within the model. In the corticosteroid-treated group, the mean level of proteinuria decreased by 5.5 g/24 hour (P = 0.01). On long-term follow-up, there was no significant difference in the incidence of hospitalizations (1 per 2.1 vs. 1 per 2.3 patient months) or of serious infections (1 per 2.6 vs. 1 per 2.3 patient months), but there was a significantly longer duration of hospitalization in the corticosteroid-treated group (3.2 vs. 2 days per patient month). At six months, only one of the non-corticosteroid-treated patients but seven of the corticosteroid-treated group continued to have independent renal function (P = 0.06). Three of the corticosteroid-treated group continued to have independent function at two years of follow-up. CONCLUSION: A limited course of corticosteroid therapy in selected patients was beneficial and safe. Further research is required for the role of corticosteroids in the treatment of HIVAN.

AIDS-Associated Nephropathy↗
PubMed2006

Elevated serum creatinine and a normal urinalysis: a short differential diagnosis in the etiology of renal failure.

OBJECTIVE: The diagnosis of renal failure with a normal urinalysis represents a short differential diagnosis that has not been characterized in the literature. This study was designed to identify the specific disease states that encompass this interesting renal condition. MATERIAL: The Regenstrief database, which is an electronic medical record containing inpatient laboratory and other clinical data for patients admitted to Wishard Memorial Hospital, was utilized to provide data for this study. METHODS: The database was culled to provide data for hospitalized patients admitted between March 1, 1992, and March 1, 2001, with the concurrent findings of a serum creatinine greater than or equal to 2 mg/dL, a normal urinalysis, and diagnoses of obstructive uropathy, multiple myeloma, prerenal azotemia, hypertensive nephrosclerosis, interstitial nephritis, renal vascular disease, hypokalemic nephropathy, and hypercalcemia, as identified by their corresponding ICD-9 codes. RESULTS: A search of the Regenstrief database yielded a total of 190,343 patient admissions. There were 515 patient admissions with renal failure and a concurrent normal urinalysis. The largest specific diagnostic categories within this group were hypertension and prerenal azotemia. CONCLUSIONS: An elevated serum creatinine and normal urinalysis present a short differential for the etiologies of renal failure and include such entities as hypertensive nephrosclerosis, prerenal azotemia, obstructive nephropathy, interstitial nephritis, renal vascular disease, and various electrolyte abnormalities. An awareness of these specific disease states may lead to an earlier diagnosis and more effective treatment of renal failure.

Creatinine↗
PubMed2002

Hypotension, renal failure, and pulmonary complications in leptospirosis.

During a recent outbreak of leptospirosis in northeastern Thailand, 148 patients with serologically diagnosed leptospirosis were seen in Loei hospital. The common serotypes were L. pyrogenes, and L. sejroe. Hypotension with a mean arterial pressure less than 70 mmHg upon admission or within 24 h after admission was observed in 94 patients or 64%. 30 patients had normal renal function; 30 patients had prerenal azotemia with mild pulmonary complication in 2; and 34 patients had acute renal failure. 29 patients with acute renal failure had pulmonary complications including pulmonary hemorrhage in 8, pulmonary edema in 3, acute respiratory distress syndrome (ARDS) in 14 and interstitial pneumonitis in 4. 54 patients had normal blood pressure. In this group 5 patients had acute renal failure; 16 had prerenal azotemia and 33 had normal renal function. Interstitial pneumonitis was noted in one patient with prerenal azotemia. Less renal complication and minimal pulmonary complication were seen in leptospirosis patients with normal blood pressure. The patients with normal renal function had no pulmonary complication. Good association existed between hypotension, renal failure and pulmonary complications.

Acute Kidney Injury↗
PubMed1986

Effect of vitamin B-6 deficiency on plasma amino acid levels in chronically azotemic rats.

Chronic renal failure is associated with many abnormalities in plasma amino acids. Since patients with renal failure are frequently deficient in vitamin B-6, this study examined whether vitamin B-6 deficiency may be a cause of any of the abnormal plasma amino acid concentrations observed in chronic renal failure. Sham-operated and chronically azotemic rats were pair-fed diets deficient in or replete with vitamin B-6 for 21 d. By the end of 21 d, the EGOT index rose significantly in the B-6-deficient rats but not in the B-6-replete animals. There were several differences in plasma amino acid concentrations between azotemic and control rats. Azotemia and B-6 deficiency each lowered the plasma serine concentration and raised the glycine-to-serine ratio. Plasma glycine was affected by a two-way interaction between azotemia and vitamin B-6 deficiency whereby the highest values were found in the sham-operated vitamin B-6-deficient animals. Plasma alanine and asparagine were reduced by B-6 deficiency and unchanged by azotemia. These results suggest that vitamin B-6 deficiency may contribute to several of the abnormalities in the plasma aminograms observed in chronic renal failure.

Amino Acids↗
PubMedDate not supplied

Continuous infusion tobramycin combined with carbenicillin for infections in cancer patients.

The cure rate of infections in cancer patients is adversely affected by neutropenia (less than 1,000/mm3). In particular, patients with severe neutropenia (less than 100/mm3) have shown a poor response to antibiotics. To overcome the adverse effects of neutropenia, tobramycin was given by continuous infusion and combined with intermittent carbenicillin. Tobramycin was given to a total daily dose of 300 mg/m2 and carbenicillin was given at a dose of 5 gm every four hours. There were 125 infectious episodes in 116 cancer patients receiving myelosuppressive chemotherapy. The overall cure rate was 70%. Pneumonia was the most common infection and 61% of 59 episodes were cured. Gram-negative bacilli were the most common causative organisms and 69% of these infections were cured. The most common pathogen was Klebsiella pneumoniae and this, together with Escherichia coli and Pseudomonas aeruginosa, accounted for 74% of all gram-negative bacillary infections. Response was not influenced by the initial neutrophil count, with a 62% cure rate for 39 episodes associated with severe neutropenia. However, failure of the neutrophil count to increase during therapy adversely affected response. Azotemia was the major side effect recognized, and it occurred in 11% of episodes. Major azotemia (serum creatinine greater than 2.5 mg/dl or BUN greater than 50 mg/dl) occurred in only 2%. Azotemia was not related to duration of therapy or serum tobramycin concentration. This antibiotic regimen showed both therapeutic efficacy and acceptable renal toxicity for these patients.

Anti-Bacterial Agents↗
PubMed1984

The role of dietary protein in the progression and symptomatology of chronic renal failure.

Dietary factors may have substantial impact on the clinical manifestations and even the progression of chronic renal failure. Proper dietary management can prevent certain uremic complications, decrease azotemia, and may even prevent the loss of residual renal function. Recent studies indicate that dietary protein may accelerate the normal age-related deterioration of renal function in rats. The extensive ablation of functional renal mass in rats leads to hyperemia and hyperfiltration in remnant nephrons. Continued hyperfiltration theoretically results in glomerular damage, proteinuria, and ultimately glomerular sclerosis. Dietary protein restriction reduces the remnant nephron hyperfiltration and reduces the rate of glomerular sclerosis, at least in the rat. The role of dietary protein in the pathogenesis of human nephrosclerosis remains controversial. Though dietary factors may or may not affect the rate of progression of renal insufficiency, there is no doubt that proper dietary management can limit or forestall uremic symptoms and the need for dialysis. Diets containing about 0.5 gm protein/kg body weight/day usually maintain a neutral or slightly positive nitrogen balance, while lesser amounts usually result in malnutrition. When protein intake exceeds 0.5 gm/kg/day azotemia increases dramatically. The use of nitrogen-free keto- or hydroxy-analogues of amino acids promotes positive nitrogen balance while reducing azotemia in patients with near-end-stage renal disease.

Amino Acids↗
PubMed1993

The spectrum of kidney diseases in patients with human immunodeficiency virus infection.

Familiarity with renal issues that can challenge the care of patients with human immunodeficiency virus (HIV) should expedite diagnosis and therapeutic interventions. Among the most common problems are electrolyte and acid-base imbalances from many opportunistic infections or their treatments, including hyponatremia, hyperkalemia, hypokalemia, and hypo- and hypercalcemia. Acid-base disturbances, simple or mixed, can be due to underlying sepsis, opportunistic infections, or the therapy thereof. A recent report of seven patients with HIV with type B lactic acidosis failed to identify a satisfactory etiology. Elevations in creatinine or diminishing urine output should alert the physician to the possibilities of prerenal azotemia or acute tubular necrosis, which can result from progression of prerenal azotemia or can occur secondary to administered nephrotoxins, such as certain antibiotics and radiocontrast agents. Agents associated with nephrotoxicity include aminoglycosides, antifungal, antiviral, and radiocontrast agents, and nonsteroidal anti-inflammatory pain medications. Although prerenal azotemia and acute tubular necrosis are the most frequent causes of acute renal failure, the differential diagnosis should include acute interstitial nephritis, obstructive nephropathy, and glomerulopathies such as hemolytic uremic syndrome, thrombotic thrombocytopenia purpura, the newly described IgA nephropathy, and, in certain populations, HIV nephropathy.

Glomerulonephritis↗
PubMedDate not supplied

Cobalt radiation with or without low-dose cisplatin for treatment of canine naso-sinus carcinomas.

The objective of this study was to determine if low-dose cisplatin could be added safely to radiation therapy for the treatment of naso-sinus carcinomas in dogs. Thirty-one dogs were evaluated; 18 of these dogs received cobalt radiation in combination with low-dose cisplatin while 13 dogs received radiation alone. No difference was observed for acute or late radiation effects. Cisplatin was administered at a dosage of 7.5 mg/m2 20 min prior to every other radiation treatment. An initial dose of 10 mg/m2 was intended but toxicity (primarily azotemia) was unacceptable. Cisplatin was administered as prescribed in 12 of 18 dogs. Cisplatin was discontinued in 2 dogs because of azotemia. In the other 4 dogs cisplatin was not administered as prescribed because the dogs were withdrawn from treatment due to disease progression or radiation effects. There was no long-term renal disease in patients who developed azotemia. The overall median survival was 433 days with 4 (12.9%) dogs still alive at the completion of the study.

Animals↗
PubMed1988

Evaluation of azotemic patients: diagnostic yield of initial US examination.

To determine whether renal ultrasound (US) is necessary in all patients with azotemia, the authors retrospectively evaluated renal US examinations in 394 azotemic patients. The patients included 119 patients considered clinically to be at high risk for postrenal urinary obstruction and 275 patients considered to be at low risk. In the high-risk population, 35 patients were found to have hydronephrosis (29%). In the low-risk population, three patients were found to have hydronephrosis (1%). In two of these patients surgical intervention resulted in reversal of the azotemia. The authors recommend that renal US be performed in all high-risk patients and in low-risk patients only if temporization and standard medical treatment do not resolve the azotemia.

Humans↗
PubMed1988

Gentamicin nephrotoxicity in the setting of acute renal hypoperfusion.

The purpose of this study is to assess interactions between acute renal hypoperfusion and aminoglycoside nephrotoxicity. One hour of renal hypoperfusion (55-60 mmHg; renal blood flow 1.6 +/- 0.13 ml/min) was created in rats by suprarenal partial aortic constriction. Gentamicin, 120 mg/kg, was given at the start of the hypoperfusion period. Rats that either received gentamicin alone or were subjected to hypoperfusion alone served as controls. Hypoperfusion alone induced mild S3 proximal tubular brush-border membrane blebbing, but it caused no enzymuria, azotemia, or tubular necrosis. Gentamicin alone induced no azotemia or tubular necrosis. However, gentamicin injected during hypoperfusion caused severe azotemia (blood urea nitrogen 94 +/- 16; creatinine 1.74 +/- 0.22 mg/dl) and extensive S3 proximal tubular necrosis without affecting renal perfusion. S1 and S2 tubular segments, the major targets of gentamicin toxicity, showed minimal damage. Hypoperfusion increased renal gentamicin uptake, but matching it in control rats induced no renal damage. In conclusion, gentamicin can precipitate hypoperfusion-induced acute renal failure. This effect appears to be due to an S3 cytotoxic effect, which converts sublethal ischemic S3 tubular injury into overt cell necrosis.

Adenine Nucleotides↗
PubMed1980

Rapid radioimmunoassay for diagnosing acute tubular necrosis.

A previously described method for recovering a proximal renal tubular epitheal antigen (HRTE-1) from normal human kidney was modified by using ion-exchange and immunoaffinity chromatography in order to create easily reproducible conditions for antigen isolation. Radioiodinated HRTE-1 was then used to establish a 3-hour, double-antibody radioimmunoassay (RIA) for the purpose of testing whether the urinary excretion of this antigen might seve as a useful marker of acute tubular necrosis (ATN). Urines from 51 patients (ATN, 22: chronic nephropathies, 24; prerenal azotemia, 5) and from 36 normal subjects were assayed for HRTE-1. 79% of ATN patients had abnormal antigen concentrations while 100% of all other urines had urine antigen concentrations within a previously established range for random normal urine samples. When used as a differential diagnostic test of either ATN versus chronic nephropathies, or of ATN versus prerenal azotemia, 90 and 81% discrimination was achieved, respectively. The majority of ATN and prerenal azotemia patients presenting with atypical conventional diagnostic parameters (urine Na, urine osmolality, urine sediment, fractional Na excretion) were correctly diagnosed by RIA. Further study of HRTE-1 excretion in acute and chronic renal diseases seems indicated, both to elucidate pathophysiologic mechanisms and to determine whether HRTE-1 is a clinically useful marker of ATN.

Acute Kidney Injury↗
PubMed1983

The role of prostaglandins in gentamicin-induced nephrotoxicity in the dog.

The effects of chronic gentamicin administration on renal function was studied in dogs receiving 4 mg/kg i.m. of gentamicin b.i.d. for 28 days. Administration of gentamicin resulted in a bimodal change in renal function. A decrease in urine osmolality was first noted on day 6 and declined progressively throughout the study. This decrease in urinary concentrating ability was preceded by a steady rise in urinary prostaglandin E2 (PGE) excretion and followed by a rise in plasma renin activity (PRA). Prior to an increase in azotemia, urinary PGE decreased precipitously while PRA continued to rise throughout the remainder of the study. The precipitous decrease in GFR was accompanied by a significant increase in FENa to seven times control. These studies suggest a dual effect of chronic gentamicin administration on renal function: (1) an early effect manifested by stimulation of urinary prostaglandin production with a concomitant loss of urinary concentrating ability and mild prerenal azotemia, and (2) a late effect, preceded by a decrease in urinary prostaglandin excretion while PRA continues to increase, and manifested by increase fractional excretion of sodium and progressive azotemia.

Acute Kidney Injury↗
PubMed2004

Retrospective evaluation of renal disease in captive black howler monkeys (Alouatta caraya).

Six of 15 (40%) inactive medical records of adult black howler monkeys (Alouatta caraya) at one zoological institution included either a pre- or postmortem diagnosis of renal disease. In these six cases, significantly abnormal hematologic and serum chemistry values were reported at onset of azotemia, onset of clinical signs, and at euthanasia. Average age of onset of azotemia was 14.8 +/- 2.9 yr, with clinical signs of disease noted at 17 +/- 4.7 yr. In four of the cases (66.6%), azotemia was documented earlier than the onset of clinical signs of renal disease. Average duration of clinical disease was 2.83 +/- 1.6 yr, with an average age at euthanasia of 18 +/- 4.7 yr. Chronic tubulointerstitial nephritis with secondary glomerular sclerosis was present in all cases. Thirteen of an additional 20 institutions in the United States that have held Alouatta caraya responded to a survey for prevalence of renal disease. These institutions showed a lower prevalence (15.1%) of renal disease in complete, inactive records, a higher prevalence of glomerulonephritis, and similar significant clinicopathologic values.

Age of Onset↗
PubMed1994

A comparison of metabolic control by continuous and intermittent therapies in acute renal failure.

Azotemia control provided by blood pump-assisted continuous hemofiltration has not been rigorously compared with that provided by intermittent hemodialysis (IHD) for critically ill patients with acute renal failure (ARF). The metabolic control achieved by continuous venovenous hemofiltration (CVVH) and IHD was compared. In ARF patients treated with CVVH (N = 11), the normalized daily dose of therapy was 0.59 +/- 0.23 (mean +/- SD) and the normalized protein catabolic rate was 1.82 +/- 0.95 g/kg per day. The serum urea nitrogen concentration (SUN) declined with CVVH from an initial value of 114 +/- 32 to 79 +/- 17 mg/dL at steady state (SUNs). The initial analysis was a theoretical comparison between CVVH azotemia control and the control that would have been provided by IHD. Simulated IHD data were generated by conventional urea kinetic methods. The peak concentration hypothesis was invoked to compare CVVH SUNs and the peak IHD SUN (SUNp). A simulated IHD frequency of five times or more weekly was required to achieve a SUNp that did not differ from the CVVH SUNs. A similar comparison between the CVVH group and a separate group of ARF patients (N = 11) who received IHD was also performed. In the latter group, the normalized protein catabolic rate and the normalized daily dose of therapy were similar to those of the CVVH group. The SUNp (101 +/- 12 mg/dL) in the IHD group was significantly higher than the mean CVVH SUNs (P < 0.05). These data suggest that intensive hemodialysis is required to provide azotemia control similar to that provided by CVVH.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1994

Fractional excretion of trace lithium and uric acid in acute renal failure.

The early distinction between prerenal azotemia, characterized by an avid proximal tubular sodium reabsorption, and ATN, in which proximal tubule function is depressed, remains an important but difficult clinical task. Indices of acute renal failure based on urinary sodium excretion may be helpful but have several limitations, among which is the use of diuretics. The effectiveness of the fractional excretion of uric acid (FEUA) and that of endogenous lithium (FELi) in the diagnosis of acute renal failure has been evaluated in an unselected group of 46 patients, 28 with prerenal azotemia and 18 with ATN. In the entire group, FELi concurred with the clinical diagnosis in 78% of the patients, whereas the fractional excretion of sodium (FENa) and FEUA were in agreement in only 63 and 50%, respectively. FELi was more sensitive to identify hemodynamic renal failure, because 93% of prerenal failure patients had a low FELi, contrasting with a low FEUA in only 68% and a low FENa in 75%. The major reason for the discrepancy between FENa and FELi was the administration of diuretics. In both acute renal failure groups, FENa was higher in the subgroups receiving diuretics. In contrast, diuretic therapy had no effect on FELi in either group. These results suggest that FELi is more accurate than either FENa or FEUA for distinguishing prerenal azotemia from ATN. The superiority of FELi appears especially relevant in patients treated with the usual diuretics.

Acute Kidney Injury↗