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PubMed2006

Clinical characteristics and outcomes of new uremic patients with extreme azotemia in southern Taiwan.

Serum creatinine (SCr) had been considered to be an important predictor of mortality in end-stage renal disease (ESRD) patients at the start of renal replacement therapy (RRT). However, the data were limited about initially extreme azotemia (EA), exclusively defined as blood urea nitrogen (BUN) > or = 300 mg/dL, SCr > or = 30 mg/dL, or both. This retrospective study was conducted to clarify the characteristics and outcome in our EA patients. We had 1682 new ESRD patients from July 1988 to December 1996. With frequency match for age, gender, and starting RRT in the same period, 20 EA patients and 60 controls were included. Fifty percent of our EA patients had unknown etiology. The EA patients had significantly lower prevalence of underlying diabetic nephropathy, and comorbid hypertension. All the EA patients had late referral to nephrologists within 4 weeks before the initiation of RRT, and 90% of them had taken Chinese herbals. The EA group had significantly higher BUN, SCr, and iron storage as well as a higher prevalence of severe anemia, hyperkalemia, hypocalcemia, and acidemia. However, the similar prevalence of cardiomegaly and left ventricular hypertrophy as well as the similar early mortality rate and long-term survival were noted. Age over 40 years, comorbid diabetes mellitus, and hypoalbuminemia were independent predictors of poor survival. Our EA patients had different initial presentations from other uremic ones at the start of RRT. However, the short-term and long-term mortality rates were similar. The lower prevalence of underlying diabetic nephropathy and comorbid hypertension among the EA patients might contribute to their fair outcome.

Adult↗
PubMed2002

Are gadolinium-based contrast media really safer than iodinated media for digital subtraction angiography in patients with azotemia?

Gadolinium chelates, intended as intravenous contrast media for magnetic resonance imaging, have been regarded as nonnephrotoxic and recommended to replace iodinated contrast media in patients with azotemia who are undergoing digital subtraction angiography (DSA). High intraarterial doses (up to 220 mmol of gadodiamide) have been used, with a 40% incidence of nephropathy. The authors discourage the use of gadolinium for DSA for several reasons. (a) There exist no randomized studies comparing the nephrotoxic effects of gadolinium-based and iodinated media at equal-attenuating concentrations and doses. (b) Gadolinium-based media are hypertonic, a pathogenetic factor in contrast medium-induced nephropathy after renal angiography, with an osmolality two to seven times that of plasma. Iodinated media in concentrations that are equally attenuating with gadolinium-based media can be made isotonic. (c) In vitro measurements indicate that 0.5 mol/L gadolinium chelates are equally attenuating with 60-80 mg iodine per milliliter at the commonly used 70-90-kV range used for DSA. Thus, 50 mL of 0.5 mol/L gadolinium chelate ( approximately 0.3 mmol/kg in an 80-kg person) would be equally attenuating with a dose of 3-4 g of iodine in an iodinated medium (eg, 50 mL iohexol at 60-80 mg I/mL or 10-13 mL at 300 mg I/mL). (d) By combining these data on attenuation and results of toxicity studies in mice, the general toxicity of gadolinium chelates may be six to 25 times higher than that of equal-attenuating doses of iodinated media at 70-kV DSA. Thus, the authors believe that at equal-attenuating doses for DSA, modern iodinated contrast media should result in a lower toxic load on the body than with presently available gadolinium chelates.

Angiography, Digital Subtraction↗
PubMed1987

Nitroprusside-induced acute azotemia.

A patient with congestive heart failure and pneumonia was begun on a nitroprusside infusion for cardiac afterload reduction. Urine output declined sharply and azotemia ensued despite little change in arterial pressure. Further evaluation supported a prerenal mechanism with dramatic recovery related to tapering and discontinuation of the nitroprusside. The mechanism of renal deterioration is possibly related to a 'steal' syndrome due to preferential dilation of vascular beds other than the renal.

Acute Kidney Injury↗
PubMed1981

Renin, aldosterone and other mineralocorticoids in hyperkalemic patients with chronic renal failure showing mild azotemia.

The role of the renin-angiotensin system in the control of aldosterone and other mineralocorticoids was studied in 9 hyperkalemic patients with chronic renal failure showing mild azotemia (group I) and 6 normokalemic patients with chronic renal failure showing creatinine clearance similar to that in group I (group II). In group I, the plasma renin activity (PRA) was significantly low and plasma aldosterone (PAC) and 18-hydroxycortisterone (18-OH-B) were also significantly reduced. In group II, PRA was normal or slightly increased, and PAC and 18-OH-B were also normal or slightly increased. Both the PAC and 18-OH-B in group I were stimulated by ACTH and angiotensin II, although the responses were less than those in group II. In 2 patients of group I where PRA moved into the normal range after administration of furosemide, the plasma 18-OH-B and PAC also reached the lower limit of normal. These results suggest that suppression of the renin-angiotensin system is probably related to functional disturbance in the conversion from B to 18-OH-B and/or 18-OH-B to aldosterone in most abnormally hyperkalemic patients with chronic renal failure.

18-Hydroxycorticosterone↗
PubMed1988

Reduced incidence of hyperkalemia and azotemia in patients receiving sulindac compared with indomethacin.

The incidence and severity of hyperkalemia and azotemia was investigated in a prospective randomized study involving 74 patients receiving either sulindac 200 mg p.o. b.i.d. or indomethacin 25 mg p.o. t.i.d. and 100 mg p.r. The mean +/- SE posttreatment increment in serum potassium was 0.8 +/- 0.1 mmol/l in patients treated by indomethacin compared to 0.5 +/- 0.1 in those receiving sulindac (p less than 0.025). The mean +/- SE posttreatment increment in blood urea nitrogen (BUN) was 3.1 +/- 0.4 mmol/l in patients on indomethacin compared to only 0.9 +/- 0.3 in patients on sulindac (p less than 0.001). In 5 patients who developed hyperkalemia while on indomethacin, changing to sulindac resulted in a sharp reduction of serum potassium in 3, and normalization of BUN in all patients. These data support the claim of a reduced risk of impaired renal function associated with the use of sulindac.

Aged↗
PubMed2005

Relationship between impaired aldosterone response to adrenocorticotropic hormone and prevalence of hemodialysis in type 2 diabetic patients without azotemia.

The present prospective observational study was designed to assess the prevalence of hemodialysis in type 2 diabetic patients with an impairment of plasma aldosterone responsiveness to adrenocorticotropic hormone (ACTH). Sixty seven patients (43 men and 24 women) were selected. The inclusion criteria were age < 65 years; presence of normoalbuminemia (serum albumin > 3.6 g/dl); and absence of azotemia (serum creatinine < or = 1.2 mg/dl in males, and < or = 1.0 mg/dl in females). Soluble alpha(1-24)-ACTH was injected intramuscularly in a single dose of 0.25 mg after overnight recumbency. The area under the aldosterone curve (aldosterone AUC) was calculated. The diabetic patients were divided into two groups according to the levels of aldosterone AUC. Patients with an aldosterone AUC in the range of 0-381 were considered poor responders (n = 31) and those with an AUC of 397-1,007 were considered good responders (n = 36). The follow-up was performed during a 144-month period. The end point of the study was the introduction of hemodialysis. A total of 14 patients (12 poor responders and 2 good responders; p < 0.001) were introduced to hemodialysis. The prevalence of hemodialysis in the poor responders (5.74 per 100 patient-years) was significantly higher (p < 0.001, log-rank test) than that in the good responders (0.68 per 100 patient-years). One possible explanation is that an inappropriate level of salt intake relative to the impaired plasma aldosterone control may have contributed to the high prevalence of risks and hemodialysis in the poor responders.

Adrenocorticotropic Hormone↗
PubMed2004

Hypocalcemia and azotemia associated with zoledronic acid and interferon alfa.

OBJECTIVE: To describe severe hypocalcemia and acute renal failure associated with zoledronic acid and interferon alfa in a patient with metastatic carcinoid tumors. CASE SUMMARY: A 39-year-old white man with metastatic carcinoid tumor tolerated treatment with subcutaneous long-acting octreotide monthly and interferon alfa 6 million units 3 times weekly for 6 months. Due to multiple bony metastases, zoledronic acid was prescribed as a monthly 4-mg intravenous infusion over 30 minutes to prevent skeletal-related events. Although the first infusion went well, the patient developed severe hypocalcemia and acute renal failure after the second zoledronic infusion. DISCUSSION: Bisphosphonates may infrequently cause symptomatic hypocalcemia, especially among patients who have vitamin D deficiency or hypoparathyroidism or receive treatment with an aminoglycoside. Our literature review suggests that zoledronic acid and interferon alfa may exert additive effects on the inhibition of osteoclasts, thus potentially precipitating hypocalcemia. Renal dysfunction may not be a direct consequence of interferon alfa. However, altered mental function due to hypocalcemia may lead to dehydration and further exacerbate renal dysfunction, a known adverse effect of zoledronic acid. Since therapeutic indications of both interferon alfa and zoledronic acid continue to expand, clinicians should be aware of these serious adverse reactions and potential interaction. Supportive treatment with hydration, calcium supplement, and oral calcitriol resulted in resolution of hypocalcemia, but only partial improvement of azotemia. CONCLUSIONS: In our patient with metastatic carcinoid tumor, treatment with zoledronic acid and interferon alfa was associated with symptomatic hypocalcemia and acute renal failure.

Adult↗
PubMed2006

Simvastatin-amiodarone interaction resulting in rhabdomyolysis, azotemia, and possible hepatotoxicity.

OBJECTIVE: To describe the fifth reported instance, as of February 15, 2006, of a severe interaction between simvastatin and amiodarone and hypothesize inhibition of CYP3A4 as the major mechanism. CASE SUMMARY: A 72-year-old white man (178 cm, 77.2 kg) with diabetes mellitus, hyperlipidemia, hypertension, and mild azotemia was hospitalized on September 21, 2004, with thigh weakness, achiness, and dark urine for 7 days. Coronary artery bypass had been performed on July 7, 2004. Amiodarone 200 mg/day was started on July 10, and simvastatin 80 mg/day was initiated on August 13. Laboratory testing on the present admission included creatine kinase (CK) 19,620 U/L (reference range 60-224), blood urea nitrogen 50 mg/dL, creatinine 2.6 mg/dL, aspartate aminotransferase (AST) 912 U/L (30-60), alanine aminotransferase (ALT) 748 U/L (30-60), urine myoglobin 71,100 microg/L (<50), and serum myoglobin 13,877 microg/L (<110). Simvastatin and amiodarone were discontinued, and the patient was hydrated with forced alkaline diuresis. Thirteen days later, his CK was 323 U/L, creatinine 1.7 mg/dL, ALT 145 U/L, and AST 37 U/L. DISCUSSION: Simvastatin is metabolized primarily by CYP3A4, and amiodarone is a recognized inhibitor of this enzyme. This may, therefore, account for the presumed drug interaction. CONCLUSIONS: An objective causal assessment suggests that rhabdomyolysis, renal failure, and possibly hepatotoxicity were probably related to an amiodarone-simvastatin interaction.

Aged↗
PubMed1999

Prerenal azotemia in a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy.

Patients with hyporeninemic hypoaldosteronism show mild to moderate renal insufficiency, with a creatinine clearance of 20-75 ml/min, and asymptomatic hyperkalemia. A low degree of sodium wasting and mild hyperchloremic metabolic acidosis are also usually present. However, severe sodium wasting and volume depletion are not typically seen unless the patient is placed on severe sodium restriction or has some other cause of extrarenal sodium loss. In fact, acute renal failure has not been reported in such patients. We describe a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy who developed recurrent episodes of acute renal failure due to prerenal azotemia during acute exacerbations of diarrhoea. In our case, despite significant hypovolemia, the renin-aldosterone axis was markedly suppressed, implying that sympathetic tone played a decisive role in renin regulation.

Aged↗
PubMed1990

Nonsteroidal anti-inflammatory drug-associated azotemia in the very old.

We conducted a prospective study in 114 elderly patients to determine the renal effects of short-term therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) in the very old. Study subjects were patients in a long-term care facility (mean age, 87 years) newly begun on a regimen of NSAID therapy. For the study group as a whole, the serum urea nitrogen level rose 1.7 mmol/L 5 to 7 days after initiation of therapy, with no significant changes in serum creatinine or potassium levels. In a comparison group of 45 patients not receiving NSAID therapy, no significant change in the serum urea nitrogen level was noted during a similar period. A subgroup of 15 patients (13%) experienced a greater than 50% increase in the serum urea nitrogen level during NSAID therapy, with a mean increase of 89% (8.6 mmol/L). A return to the baseline level occurred within 14 days after discontinuation of NSAID therapy. Two factors were significantly predictors of a greater than 50% increase in the serum urea nitrogen level: concurrent loop diuretic therapy (odds ratio, 2.2) and high NSAID dose (odds ratio, 2.0). These findings suggest that reversible azotemia develops in a sizable proportion of the very old who are treated with short-term NSAID therapy.

Aged↗
PubMedDate not supplied

Azotemia during chronic converting enzyme inhibition with enalapril in sodium-depleted rats: role of renal circulatory changes.

Chronic administration of the angiotensin-converting enzyme inhibitor enalapril to sodium-restricted rats causes azotemia and elevations in serum creatinine. This study was undertaken to determine the contribution of altered systemic and renal hemodynamics to the reductions in renal function in sodium-restricted rats treated with enalapril. Animals were maintained for 21 days on a sodium-restricted diet (0.04 +/- 0.01 mEq Na+/24 h). Enalapril was administered in the drinking water (300 mg/L) to half the rats. Regional blood flows were measured in animals anesthetized with pentobarbital (50 mg/kg, i.p.) using the radioactive microsphere technique. Converting enzyme inhibition (CEI) reduced mean arterial pressure (130.8 +/- 5.9 vs 60.3 +/- 6.1 mm Hg, p less than 0.001), and increased cardiac index (346 +/- 33 vs. 437 +/- 28 ml/min/kg, p less than 0.05). Total peripheral resistance was significantly lower in enalapril-treated rats [0.406 +/- 0.049 vs. 0.166 +/- 0.013 arbitrary resistance units (RU), p less than 0.001]. Renal blood flow was maintained (control, 2.93 +/- 0.21 vs. enalapril, 2.55 +/- 0.28 ml/min/100 g, p = NS) despite a 54% decrease in perfusion pressure due to decreased renal vascular resistance (42.6 +/- 1.7 vs. 25.2 +/- 2.9 RU, p less than 0.001). CEI reduced coronary blood flow (2.76 +/- 0.22 vs. 1.59 +/- 0.19 ml/min/100 g, p less than 0.001), but did not change coronary vascular resistance (50.2 +/- 4.6 vs. 44.0 +/- 4.3 RU, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

[On postoperative azotemia in geriatric surgery: significance, risk groups, possibilities of prophylaxis (author's transl)].

1032 Interventions on geriatric patients beeing more than 70 years old between 1966 and 1975 demonstrate the significance of azotemia in the postoperativ stage of the disease appears as well as its dependence upon prehospital factors, type and localisation also on the extension and duration on the intervention in each single case. Since it is hardly possible to exert an influence on the preliminary stress due to the old age and on the dysfunction determined by involution of the parenchymatose organs important for the course of the postoperative stage, a particular emphasis should be laid upon the prophylactic aspekt to the purpose of an appropriate screening against vegetativ-visceral, renally effective shock reflexes (hepatorenal syndrome) and on the other, usually extra-renal factors (PH 203R, splanchnic block). Further possibilities: considerate elimination of pain and general anesthesia, purpuseful and quick operative technique, improvement of the apparatus and instruments, after-treatment specific for the given case so as one consisting of a prophylaxis against pneumonia through a rapid reactivation of the operated person. However, regardless to all the professional advance made in this field, the primary human approach to the aged patient and to his life expectancy should be made due allowance for.

Age Factors↗
PubMed1979

Pre-renal azotemia mimicking chronic renal failure in a hypotensive patient.

A 56-year-old Samoan man with a documented history of hypertension, who presented with atrial fibrillation and hypotension, quickly developed renal failure with a serum urea nitrogen of 1.370 g/L and a serum creatinine of 92 mg/L. After hydration of the patient, the creatinine value became normal in two days, the urea nitrogen in four days. The urinary creatinine output during the first 24 h of hospitalization was 3.7 g. This case illustrates the rapidity with which unusually large amounts of creatinine (more commonly seen in chronic renal failure) can accumulate and be excreted in pre-renal failure. It also reaffirms the usefulness of the urea nitrogen/creatnine ratio in evaluating the causes of azotemia.

Blood Urea Nitrogen↗
PubMed1980

Radioimmunoassay of creatine kinase B-isoenzymes in serum of patients with azotemia, obstructive uropathy, or carcinoma of the prostate or bladder.

We measured the concentrations of creatine kinase B-isoenzymes by radioimmunoassay in 271 serum specimens from patients with azotemia, benign prostatic hyperplasia, adenocarcinoma of the prostate, and transitional cell carcinoma of the bladder. There was no correlation between the concentrations of B-isoenzymes and creatinine in the sera of azotemic patients. Above-normal concentrations of B-isoenzymes were found in sera from three patients with acute renal failure, but in only two of 28 specimens from patients with chronic renal failure. Above-normal concentrations of B-isoenzymes also were found in sera from three of 18 patients with untreated carcinoma of the prostate, 10 of 25 patients with treated carcinoma, 20 of 135 patients with benign prostatic hyperplasia, and 10 of 33 patients and with transitional cell carcinoma of the bladder. An above-normal concentration of B-isoenzymes in serum has a low predictive value for adenocarcinoma of the prostate, was not a sensitive indicator of the presence of carcinoma, and was noted paradoxically in six patients with treated carcinoma who had normal acid phosphatase activities in serum. We conclude that routine measurement of B-isoenzymes is not useful to establish the diagnosis of adenocarcinoma of the prostate.

Adenocarcinoma↗
PubMed1982

Nephelometric determination of serum amylase and lipase in naturally occurring azotemia in the dog.

Serum amylase and lipase were measured in 32 healthy dogs and in 55 dogs with serum urea nitrogen values greater than 40 mg/dl, using a nephelometric analyzer (Coleman analyzer model 91). Mean serum amylase and lipase values in normal dogs were 1,085.48 units and 3.98 units, respectively. In dogs with azotemia, the mean serum amylase and lipase values were 1,822.79 units and 12.57 units, respectively. Serum urea nitrogen values could not be correlated with amylase or lipase values.

Amylases↗
PubMed1984

Effect of immunosuppressive drug therapy on blood urea nitrogen concentration in dogs with azotemia.

Azotemic dogs receiving prednisone and azathioprine to enhance renal allograft survival had higher blood urea nitrogen (BUN):serum creatinine (SC) ratios, when compared with nontreated dogs with induced azotemia. The difference in ratios probably was attributable to increased BUN content secondary to the catabolic effects of the drugs used. However, dogs with naturally occurring renal failure had BUN:SC ratios that were similar to those for dogs receiving the catabolic drugs. It was concluded that even though catabolic drugs may influence BUN:SC ratios, the multiplicity of other factors affecting BUN and SC may interact to cause a wide range of BUN:SC ratios under conditions of naturally occurring primary renal failure in the dog.

Animals↗
PubMed1980

Metabolism and rate of elimination of digoxigenin bisdigitoxoside in dogs before and during chronic azotemia.

The purpose of this study was to evaluate the metabolism and rate of elimination of digoxigenin bisdigitoxoside (bis) before and during chronic azotemia in dogs. Bis was eliminated primarily by nonrenal mechanisms. The half-life of bis was 18.5 hr, compared to 31.6 hr for digoxin, and was not significantly increased in azotemic dogs. The oral bioavailability of bis in azotemic dogs relative to an intravenous dose was approximately 46%.

Animals↗