Increased fractional excretion of sodium in prerenal azotemia: need for careful interpretation.
Explore the source record for details and available documents.
Acute Kidney Injury↗
SEARCH · Search PubMed
Results for “Azotemia”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[The progression rates of different morphological forms of chronic glomerulonephritis in the pre-azotemia period (is the morphological form of chronic glomerulonephritis the factor that determines the prognosis?)].
The multivariate analysis of overall clinicomorphological symptoms in 121 patients with chronic glomerulonephritis (CGN) allowed formulation of independent prognostic factors indicative of the time to chronic renal failure. Similar for diverse morphological CGN forms prognostic characters are those of CGN aggravation frequency, arterial hypertension, serum creatinine concentration, the pattern of tubulointerstitial changes at the time of renal biopsy. The speed of CGN morphological variants is approximately the same in similar expression of prognostically significant characters.
Adult↗
[Essential amino acids in parenteral feeding in so-called postoperative azotemia].
Explore the source record for details and available documents.
Amino Acids, Essential↗
Renal effects of angiotensin converting enzyme inhibitors in heart failure: a clinician's guide to minimizing azotemia and diuretic-induced electrolyte imbalances.
Angiotensin converting enzyme (ACE) inhibitors have proved to be valuable, life-saving medications in the management of heart failure. While reducing myocardial oxygen consumption, they increase cardiac output and thus renal plasma flow. Despite reports in the literature of adverse effects of these drugs on renal function, the risks of functional deterioration are predictable in patient populations and remediable. Patients at greatest risk of declining renal function during therapy with ACE inhibitors are those in whom maintenance of renal function is dependent on angiotensin II. Reducing the dose of the concomitant diuretic, liberalizing the dietary intake of sodium, and increasing the dose of the ACE inhibitor usually restores renal function to baseline. In patients with severe renal insufficiency, reducing the dose of the ACE inhibitor might be necessary to preserve the glomerular filtration rate.
Angiotensin-Converting Enzyme Inhibitors↗
[The reaction of the kidneys and acid-base and osmotic homeostasis to moderate physical exertion in patients with chronic pyelonephritis in the pre-azotemia period].
Bicycle ergometry (BE) up to submaximal heart rate provoked moderate metabolic acidosis in 52 patients with chronic pyelonephritis (CP) in preuremic stage. Similar changes in acid-base balance following BE were noted in 14 patients with chronic glomerulonephritis (CGN). BE in CP promoted the reduction in diuresis and fraction water excretion, elevation of creatinine concentration in the urine and its concentration index in the absence of alterations in sodium and osmotic homeostasis. In CGN BE induced similar changes but an insignificant decrease in diuresis and a significant rise in serum sodium concentrations, osmolality of the urine, osmotic concentration index, absolute reabsorption of osmotically free water, fall in excreted sodium fraction. It is suggested that the above differences in the response to exercise test in CP and CGN may relate to tubulointerstitial nature of CP.
Acid-Base Equilibrium↗
Therapy of membranous nephropathy with severe azotemia.
Explore the source record for details and available documents.
Aged↗
Diagnostic exercise: azotemia in a rabbit (Oryctolagus cuniculus).
Explore the source record for details and available documents.
Anesthetics↗
[Pulmonary complications of azotemia. A case of uremic lung].
The authors studied the problem of pulmonary complications in acute and chronic uremia. They recalled the main characteristics of haemodynamic oedemas which can accompany the periods of left ventricular insufficiency during the evolution of uremia. They analized the characteristicsof the classic uremic lung representing in fact only a variety of lesional oedema in which the toxic effect of urea is controversial. Ventilatory consequences of chronic uremia were briefly exposed.
Capillary Permeability↗
Evaluation of blood urea nitrogen and serum creatinine concentrations as indicators of renal dysfunction: a study of 111 cases and a review of related literature.
Blood urea nitrogen concentration (BUN), serum creatinine concentration (SC), and BUN/SC ratios, as recorded for 111 dogs and cats with azotemia, were evaluated to determine their usefulness in evaluation of renal dysfunction. Cases were categorized into prerenal, renal, and post-renal causes of azotemia, on the basis of histologic and clinical criteria. The severity of azotemia varied within groups, but the mean value for degree of azotemia was lowest in the prerenal group. The BUN/SC ratios were highest when azotemia was mild, regardless of cause. The BUN/SC ratios in the 3 groups were not significantly different when the degree of azotemia was considered, indicating that differentiation of renal from extrarenal azotemia was not possible in the dog and cat, on the basis of relative values of BUN and SC. Comparison of BUN/SC ratios in acute and chronic azotemia of comparable magnitude revealed no significant differences between groups, indicating that this ratio cannot be used to differentiate acute and chronic azotemia. Following supportive therapy, BUN decreased significantly (P less than 0.05) more than SC, suggesting that extrarenal factors contributed to the increased BUN and that proportionately more urea than creatinine was excreted by the kidneys during therapy. The BUN/SC ratios varied widely and to a similar degree in all groups examined. Inasmuch as the BUN and SC were not correlated with more accurate measurements of renal function, conclusions could not be drawn concerning the superiority of either factor as a measure of renal function. Many nonrenal factors, previously identified, influence serum concentration of urea and creatinine. In recent studies involving azotemic human beings and rats, it was suggested that up to 25% of the urea and 65% of the creatinine produced in the body is degraded by enteric bacteria rather than excreted directly by the kidneys. These data indicate that neither BUN or SC can be used as precise tests of renal function, although SC is subject to alteration by fewer nonrenal factors than is BUN. In older medical and veterinary medical literature, the use of SC as a prognostic indicator had been advocated. Newer findings on the pathophysiology of creatininemia and retrospective case studies do not support this view. In the present study, severe creatininemia was documented in cases in which primary renal dysfunction did not exist. It was concluded that BUN and SC should continue to be regarded as crude indexes of renal function. Clinical value lies in the relative ease of their determination. Because of their lack of sensitivity, more specific evaluation of renal function (urine concentrating ability, phenolsulfonphthalein excretion) may be indicated when BUN and SC are normal or only slightly elevated. Because extrarenal factors may alter BUN and SC, it is necessary to correlate these values with clinical and other laboratory data to differentiate renal from extra-renal azotemia. Single determinations of BUN or SC provide no basis for prognosis.
Animals↗
Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas.
The early metabolic events in 33 patients with non-Hodgkin lymphoma were analyzed in the present study. Twenty-three patients had Burkitt lymphoma, 3 had non-Burkitt undifferentiated lymphoma and 7 had lymphoblastic lymphoma. Eight patients developed azotemia prior to starting chemotherapy while five did so during the first treatment week. All the patients but two who developed azotemia had stage C or D disease. Serum LDH prior to chemotherapy correlated well with the stage of disease and predicted the serum levels of creatinine, uric acid and phosphorus in the post-treatment period. Surgical excision of the main tumor mass was associated with a low incidence of azotemia and other metabolic derangements. Hyperuricemia and occasionally obstruction were encountered as the causes of azotemia in the pre-treatment period. Hyperuricemia and/or hyperphosphatemia were presumed responsible for the development of azotemia in the post-chemotherapy period. Two patients were dialyzed for renal failure due to hyperuricemia and one for renal failure due to hyperphosphatemia which developed shortly after starting chemotherapy. The patterns of renal and metabolic disturbances observed during treatment of these patients were characterized by the following profiles: 1. Azotemia due to hyperuricemia prior to treatment. 2. Hyperuricemia without azotemia in the pre-treatment period with azotemia due to hyperphosphatemia in the post-treatment period. 3. Azotemia due to combined hyperphosphatemia and hyperuricemia developing gradually in post-treatment period. 4. Increased urine phosphorus excretion in both non-azotemic and azotemic patients.
Adolescent↗
Clinical and clinicopathologic abnormalities in greyhounds with cutaneous and renal glomerular vasculopathy: 18 cases (1992-1994)
OBJECTIVE: To determine clinical signs and clinicopathologic abnormalities in Greyhounds with cutaneous and renal glomerular vasculopathy and to determine whether there were any differences between dogs with and without renal azotemia. DESIGN: Retrospective study. ANIMALS: 18 Greyhounds. PROCEDURE: Results of CBC, serum biochemical analyses, urinalyses, coagulation tests, tests of RBC morphology, bacterial culture of blood samples, and serologic tests for Rickettsia rickettsii, Ehrlichia canis, E platys, and Leptospira interrogans were reviewed. Glomerular filtration rates and urine protein:creatinine ratios were determined in most dogs. t-Tests and a test of equality of proportions were used to compare dogs that developed renal azotemia with dogs that did not. RESULTS: None of the dogs was bacteremic or had serologic evidence of infectious disease. Ten dogs had renal azotemia, 16 had anemia, 11 had hypoalbuminemia, and 18 developed thrombocytopenia. Compared with dogs without renal azotemia, dogs with renal azotemia had significantly lower mean platelet count, hematocrit, and serum albumin concentration and significantly higher mean neutrophil count and creatine kinase activity. All 10 dogs with renal azotemia died or were euthanatized; 7 of 8 dogs without azotemia survived. CLINICAL IMPLICATIONS: Greyhounds with cutaneous and renal glomerular vasculopathy that developed renal azotemia had evidence of more severe systemic disease than did dogs that did not have azotemia and, despite supportive treatment, had a poorer prognosis.
Alanine Transaminase↗
The effects of dehydration on rehabilitation outcomes of elderly orthopedic patients.
OBJECTIVE: To study the effects of dehydration, by using the indices of prerenal azotemia and orthostasis, on the rehabilitation outcomes of elderly orthopedic patients. DESIGN: Prospective, pilot study. SETTING: Regional inpatient rehabilitation center. PARTICIPANTS: A consecutive sample of 39 patients (29 women, 10 men), ranging in age from 58 to 94 years (mean, 78y), of whom 13 had total hip replacements, 12 had total knee replacements, and 14 had hip fractures. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Length of stay (LOS), change in the FIM trade mark instrument score, and discharge to home. RESULTS: The mean LOS was significantly longer in the group with prerenal azotemia (n=21, 12.9+/-3.0d, t=2.49, P<.01) than in the nonazotemic group (n=18, 9.4+/-4.6d). LOS was also significantly longer in the orthostatic group (n=18, 13.7+/-3.4d, t=2.94, P<.01) than in the nonorthostatic group (n=21, 9.8+/-3.9d). Two-way analysis of variance showed a statistically significant effect on LOS for both azotemia (F=8.4, P=.006) and orthostasis (F=10.5, P=.003). A statistical interaction existed (F=4.7, P=.038), but it was more pronounced in the absence of both conditions, as opposed to the presence of both. LOS for the group with both azotemia and orthostasis was 13.6+/-2.7 days (n=10, F=4.7, P=.038), in contrast to 7.2+/-2.8 days in the group without either condition (n=10). Of the patients who had neither azotemia nor orthostasis, 100% (n=10) went home; 80% (n=8) of patients who had both conditions went home. Logistic regression analysis, however, did not show a statistically significant correlation between discharge to home and the presence of azotemia, orthostasis, or both. CONCLUSION: Prerenal azotemia and orthostasis are present in a significant number of elderly orthopedic patients and have a major effect on rehabilitation outcomes.
Aged↗
Modification of disease progression in rats with inherited polycystic kidney disease.
The most common inherited form of human polycystic kidney disease (PKD), autosomal dominant PKD (ADPKD), is a leading cause of chronic renal failure, but has a variable clinical presentation, with end-stage renal disease occurring in only 25% to 75%. Several findings are consistent with the idea that factors in addition to the primary mutation can affect the progression of cystic change and chronic renal failure in PKD. Epithelial cell proliferation is a central element in the pathogenesis of renal cysts. We postulated that the superimposition of a growth-promoting stimulus might promote more intense proliferation of cystic epithelial cells in inherited cystic disease. To study this, we subjected Han:SPRD rats, with a form of ADPKD that resembles human ADPKD, from 4 until 10 weeks of age to diets designed to promote tubule cell growth. The diets included supplemental NH4Cl (280 mmol/L in drinking water), limited dietary K+ (0.016% of diet; control diet was 1.1% K+), and increased dietary protein (50%; control diet was 23% protein). Treatments designed to promote cell growth caused more aggressive PKD in males and females, worsened azotemia in males, and resulted in azotemia in females (which normally develop PKD but not azotemia at the ages studied). NH4Cl, K+ restriction, and increased dietary protein each caused greater kidney enlargement in males (kidney weight/body weight ratios increased by 35%, 78%, and 105%, respectively) and worsened azotemia in males (serum urea nitrogen values increased by 63%, 514%, and 224%, respectively); in contrast, decreased dietary protein (4%) caused less severe PKD in males (kidney weight/body weight ratios decreased by 43%) and lessened azotemia in males (serum urea nitrogen values decreased by 49%). Similarly, NH4Cl and K+ restriction caused greater kidney enlargement in females (kidney weight/body weight ratios increased by 206% and 203%, respectively) and caused azotemia in females (serum urea nitrogen values increased by 177% and 430%, respectively). On the basis of these results, we conclude that growth-promoting stimuli can alter the expression of hereditary renal cystic disease. These findings demonstrate that the progression of hereditary renal cystic disease can be altered by factors in addition to the primary genetic defect.
Ammonium Chloride↗
Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure.
BACKGROUND: Fractional excretion of sodium (FENa) has been used in the diagnosis of acute renal failure (ARF) to distinguish between the two main causes of ARF, prerenal state and acute tubular necrosis (ATN). However, many patients with prerenal disorders receive diuretics, which decrease sodium reabsorption and thus increase FENa. In contrast, the fractional excretion of urea nitrogen (FEUN) is primarily dependent on passive forces and is therefore less influenced by diuretic therapy. METHODS: To test the hypothesis that FEUN might be more useful in evaluating ARF, we prospectively compared FEUN with FENa during 102 episodes of ARF due to either prerenal azotemia or ATN. RESULTS: Patients were divided into three groups: those with prerenal azotemia (N = 50), those with prerenal azotemia treated with diuretics (N = 27), and those with ATN (N = 25). FENa was low only in the patients with untreated plain prerenal azotemia while it was high in both the prerenal with diuretics and the ATN groups. FEUN was essentially identical in the two pre-renal groups (27.9 +/- 2.4% vs. 24.5 +/- 2.3%), and very different from the FEUN found in ATN (58.6 +/- 3.6%, P < 0.0001). While 92% of the patients with prerenal azotemia had a FENa <1%, only 48% of those patients with prerenal and diuretic therapy had such a low FENa. By contrast 89% of this latter group had a FEUN <35%. CONCLUSIONS: Low FEUN (</=35%) was found to be a more sensitive and specific index than FENa in differentiating between ARF due to prerenal azotemia and that due to ATN, especially if diuretics have been administered.
Acute Kidney Injury↗
Urinary measurement of Na+/H+ exchanger isoform 3 (NHE3) protein as new marker of tubule injury in critically ill patients with ARF.
BACKGROUND: It has been shown that apical sodium transporters of the renal tubule can be detected by immunoblotting of urine membrane fraction from rats. We raised the hypothesis that protein levels of the Na+/H+ exchanger isoform 3 (NHE3), the most abundant apical sodium transporter in renal tubule, should be increased in urine of patients presenting with acute renal failure (ARF) with severe tubular cell damage and thus might be a noninvasive marker of acute tubular necrosis (ATN). METHODS: Sixty-eight patients admitted to the intensive care unit were studied prospectively (54 patients with ARF, 14 controls without renal dysfunction). Patients with ARF were divided into 3 subgroups as follows: prerenal azotemia, ATN, and intrinsic ARF other than ATN. Urinary NHE3 protein abundance was estimated from semiquantitative immunoblots of urine membrane fraction samples collected from patients. The amount of urinary NHE3 was compared with the fractional excretion of sodium (FeNa) and urinary retinol-binding protein (RBP). RESULTS: NHE3 was not detected in urine from controls. Levels of urinary NHE3 normalized to urinary creatinine level were increased in patients with prerenal azotemia and 6 times as much in patients with ATN, without overlap (ATN, 0.78 +/- 0.36; prerenal azotemia, 0.12 +/- 0.08; P < 0.001). Conversely, urinary NHE3 protein was not detected in patients with intrinsic ARF other than ATN. Normalized NHE3 level correlated positively with serum creatinine level in patients with tubular injury (R2 = 0.305; P = 0.0003). Values for FeNa and normalized urinary RBP did not discriminate ATN from intrinsic ARF other than ATN and prerenal azotemia, respectively. CONCLUSION: In patients with ARF, urinary NHE3 abundance might be a novel noninvasive marker of renal tubule damage, helping to differentiate prerenal azotemia, ATN, and intrinsic ARF other than ATN.
APACHE↗
Ischemic renal disease: an emerging cause of chronic renal failure and end-stage renal disease.
Ischemic renal disease (IRD) is defined as a clinically important reduction in glomerular filtration rate or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents itself in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. Eleven to 14% of end-stage renal disease (ESRD) cases are attributable to chronic IRD. A high percentage of patients entering ESRD programs are hypertensive. Many patients with a presumed diagnosis of hypertensive nephrosclerosis actually have undiagnosed ischemic nephropathy as the etiology of their ESRD. It is important for the clinician to identify IRD, because IRD is a potentially reversible cause of chronic renal failure in a hypertensive patient. Atherosclerotic renal artery disease is common among patients with coronary artery disease and aortic and peripheral vascular disease. Atherosclerotic renal artery disease is a progressive disorder, and its progression is associated with loss of renal mass and functioning. A decrease in glomerular filtration rate sufficient to cause an elevation of the serum creatinine concentration requires injury to both kidneys. Consequently, IRD can arise from one of two main clinical situations: bilateral hemodynamically significant renal artery stenosis leading to bilateral renal ischemia; and hemodynamically significant renal artery stenosis in a solitary functioning kidney, or in a kidney that is providing the majority of a patient's glomerular filtration. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function, or a delay in progression to ESRD. There are six major clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed upon poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. Noninvasive testing modalities that have been used recently include the angiotensin converting enzyme inhibitor renal scan, duplex Doppler sonography, magnetic resonance angiography, and the spiral computed tomography. Treatment methods include percutaneous transluminal angioplasty, endovascular stenting, and surgical revascularization. The results of treatment for preservation of renal function have been encouraging, with stabilization or improvement in renal function observed in a significant proportion of cases.
Humans↗
University of Miami Division of Clinical Pharmacology Therapeutic Rounds: ischemic renal disease.
Ischemic renal disease (IRD) is defined as a significant reduction in glomerular filtration rate and/or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. IRD is an important cause of chronic renal failure and end-stage renal disease (ESRD), and many patients with a presumed diagnosis of hypertensive nephrosclerosis may actually have undiagnosed ischemic nephropathy as the cause of their ESRD. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function or a delay in progression to ESRD. There are six typical clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin-converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed on poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. It is important for the clinician to identify IRD, because IRD represents a potentially reversible cause of chronic renal failure in a hypertensive patient.
Aged↗
von Willebrand factor is not altered in azotemic dogs with prolonged bleeding time.
The effects of azotemia on von Willebrand factor (vWf) plasma concentration, structure, and function were studied by utilizing canine models for both uremic bleeding and type I vWf deficiency (vWd). Seventy-five percent to 80% renal mass reduction in eight mixed-breed dogs induced marked azotemia (blood urea nitrogen [BUN] 103 +/- 7 mg/dl [mean +/- SEM]; creatinine 5.8 +/- 1 mg/dl) and prolonged mean buccal mucosal bleeding time (BMBT) from 1.8 +/- 0.2 minutes to 7.0 +/- 0.4 minutes. The mean vWf plasma concentration increased from 0.88 +/- 0.11 U/ml to 1.26 +/- 0.14 U/ml. The pre- and postsurgical sodium dodecyl sulfate-agarose gel electrophoresis multimeric patterns were similar in all dogs. Administration of cryoprecipitate from pooled azotemic mixed-breed dog plasma to five Doberman pinschers with type I vWd increased the mean plasma vWf from 0.14 +/- 0.01 U/ml to 0.48 +/- 0.04 U/ml and decreased the BMBT from 7.1 +/- 0.6 minutes to 3.14 +/- 0.09 minutes. After renal mass reduction, five type I vWd Dobermans developed marked azotemia (BUN 79 +/- 8.6 mg/dl; creatinine 3.7 +/- 0.6 mg/dl) and prolonged BMBT (16.1 +/- 3.6 minutes). Findings in the eight azotemic mixed-breed dogs indicated that (1) vWf plasma levels were normal to increased in azotemic dogs; (2) vWf structure and multimeric distribution were not altered in canine azotemia; and (3) vWf was functional when placed in a non-azotemic environment. The prolongation of the BMBT in azotemic vWd dogs indicated that factors other than alteration of vWf function were responsible for the prolonged BMBT in canine azotemia.
Animals↗