Search PubMed⌕ Search

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.

At least 487 records · Page 27Linked to original sources
PubMed1969

Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study.

Toxemia was induced in 13 of 20 pregnant ewes by the stress of a change in environment and food deprivation late in pregnancy. Of the toxemic ewes, eight developed prominent neurological findings with convulsions, motor weakness, and blindness, whereas five ewes developed azotemia without neurological signs. Proteinuria and azotemia occurred in all but one of the toxemic animals. Seven animals did not develop clinical or laboratory evidence of toxemia. Hypertension did not occur with the onset of toxemia but all toxemic animals showed glomerular changes by light and electron microscopy. These abnormalities, which were similar to those seen in human preeclampsia, included endothelial cell swelling, focal reduplication of the basement membrane, and fusion of the epithelial cell foot processes. The toxemia could not be attributed to changes in hematocrit, plasma glucose, Na, Cl, CO(2), K, Ca, fibrinogen, arterial pH, lactate, or pyruvate concentrations. Cardiac output fell only in ewes with prominent neurological signs. Plasma renin rose strikingly in animals developing toxemia, without change in substrate concentration. In contrast to human and other species, sheep uterus and amniotic fluid contained no detectable quantities of renin. Thus in response to stress the pregnant ewe develops a toxemia which in the absence of hypertension has clinical and pathological similarities to human preeclampsia.

Adrenal Glands↗
PubMed1970

Serum and urinary proteins, lysozyme (muramidase), and renal dysfunction in mono- and myelomonocytic leukemia.

Serum levels, urinary excretion, and clearances of several proteins of different molecular weights were studied in 18 patients with mono- and myelomonocytic leukemia. Nine patients had normal renal function (group A) and nine had impaired renal function with azotemia (group B). The majority of patients in both groups had increased concentration of immunoglobulins, particularly IgG, IgA, and IgM; IgD level was normal. Serum transferrin and alpha(2)-macroglobulin were frequently reduced while the level of ceruloplasmin was often increased, especially in patients with azotemia. The activity of lysozyme in the serum was high in all patients, but was considerably higher in group B. Proteinuria was found in most patients but was more prominent in group B. Almost invariably albumin constituted less than 25% of the total protein excreted. Qualitative analysis of various urinary proteins by immunochemical techniques and clearance studies suggested the presence of glomerular as well as tubular dysfunction. Determination of urinary lysozyme frequently showed no direct correlation between the serum level of the enzyme and its concentration in the urine or its clearance by the kidney. In addition to glomerular filtration, impaired tubular reabsorption may account for the high level of lysozyme in the urine. It is postulated that the very high level of lysozyme in the glomerular filtrate and possibly hypergammaglobulinemia may play a role in the induction of tubular damage. Renal impairment has been correlated with histological changes in the kidneys. From a comparative study of various leukemias, it seems that the combined glomerular-tubular dysfunction is a manifestation unique to mono- and myelomonocytic leukemia.

Adult↗
PubMed1981

Effect of thyroparathyroidectomy and parathyroidectomy on renal function and the nephrotic syndrome in rat nephrotoxic serum nephritis.

Dietary phosphorus restriction (PR) prevents uremia in rats with nephrotoxic serum nephritis (NSN). One possible mechanism by which PR could be protective would be through the suppression of parathyroid hormone. To evaluate this possibility two separate protocols were designed. In the first rats were thyroparathyroidectomized (TPTX) before (n = 11) or 5 wk after (n = 7) NSN induction and compared to sham-operated parathyroid intact rats with NSN (n = 12). At the end of the 23-wk study, intact rats were azotemic, plasma creatinine 3.80+/-0.81 mg/100 ml vs. 0.65+/-0.07 for TPTX rats (P < 0.001). During the study 75% of intact rats died of uremia in contrast to none of the TPTX rats (P < 0.001). Renal histological damage was greatly diminished and calcification prevented in TPTX rats. The proteinuria of the heterologous phase was unaffected, but the protein excretion and hypertriglyceridemia (HTG) of the autologous phase were markedly decreased in the TPTX rats. The degree of HTG and proteinuria had a high positive correlation (P < 0.001). Late TPTX also produced significant decreases in proteinuria and HTG regardless of the degree of azotemia, and prevented azotemia if the plasma creatinine at the time of TPTX was </=0.85 mg/100 ml. In additional studies selective parathyroidectomy (PTX) was performed. The adequacy of this procedure was documented by showing a similar fall in plasma Ca and urinary cyclic AMP in PTX animals as found in TPTX animals. However, selective PTX had no effect on proteinuria, histologic damage, or functional deterioration. These studies further showed that early, histologic damage and functional deterioration preceeded renal parenchymal calcification. Because animals were pair fed and both groups were given 1,25-dihydroxycholecalciferol to normalize serum Ca and P levels these studies exclude alterations in plasma Ca and P levels, dietary intake, urinary P excretion, and vitamin D administration in promoting the protective effect of TPTX on renal function. We conclude that TPTX is equally effective in preventing functional deterioration and more effective in reducing proteinuria in NSN than PR. The mechanism of this protective effect remains to be elucidated, since it does not primarily involve either the elimination of parathyroid hormone or the prevention of renal parenchymal calcification.

Animals↗
PubMed1986

Gentamicin and gram-negative bacteremia. A synergism for the development of experimental nephrotoxic acute renal failure.

To explore whether bacteremia potentiates gentamicin nephrotoxicity, we injected rats with either 1 X 10(9) Escherichia coli (E. coli), Pseudomonas aeruginosa, or Staphylococcus aureus, and then gave them gentamicin, 100 mg/kg. Renal injury was assessed over the next 24-48 h. Staphylococcus/gentamicin or gentamicin alone induced no renal injury. However, E. coli/gentamicin and Pseudomonas/gentamicin caused acute renal failure (severe azotemia; tubular necrosis; cast formation). This effect was not due to acute reductions in arterial blood pressure or renal blood flow, it could be reproduced by substituting nonviable for viable gram-negative organisms, and it was associated with increased renal gentamicin uptake. E. coli without gentamicin induced only mild azotemia and no tubular necrosis. Endotoxin-tolerant rats were significantly protected against the E. coli/gentamicin nephrotoxic interaction. We conclude that gram-negative bacteremia and gentamicin exert synergistic nephrotoxicities; and that this effect is mediated, at least in part, by endotoxin and in part by increased renal gentamicin uptake.

Acute Kidney Injury↗
PubMedDate not supplied

The effect of vitamin B6 deficiency on food intake, growth, and renal function in chronically azotemic rats.

Chronically uremic patients appear to have an increased nutritional requirement for vitamin B6, and vitamin B6 deficiency occurs frequently when such individuals do not receive supplements of this vitamin. Since manifestations of vitamin B6 deficiency in renal failure are not well defined, this study examined two aspects of the chronic renal failure syndrome which might be influenced by vitamin B6: impaired growth and progressive loss of renal function. We examined food intake, weight gain, the food efficiency ratio, degree of azotemia, and renal function in chronically azotemic rats pair-fed for 6 weeks either a vitamin B6-deficient diet or a diet containing a surfeit of vitamin B6. In the azotemic vitamin B6-deficient rats, as compared to the azotemic B6-replete rats, there was evidence of reduced appetite, decreased weight gain, a lower food efficiency ratio, increased azotemia, and a reduced glomerular filtration rate as estimated from the urea clearance or the mean of the urea and creatinine clearances. These findings suggest that vitamin B6 deficiency may contribute to decreased food intake, reduced growth, and lower renal function in animals with chronic renal insufficiency.

Animals↗
PubMedDate not supplied

Gastrointestinal, hepatic, and metabolic effects of enteral and parenteral nutrition in rats infused with tumor necrosis factor.

BACKGROUND: We previously showed that continuous infusion of tumor necrosis factor-alpha (TNF-alpha) in orally fed rats caused weight and muscle wasting mainly because of anorexia. However, when we tried to prevent weight loss by giving total parenteral nutrition (TPN), TNF-infused rats developed hyperglycemia, azotemia, and hepatic abnormalities. The present study was designed to determine whether the enteral (ENT) feeding resulted in fewer complications than parenteral (TPN) feeding in TNF-infused rats (100 micrograms/kg/d). METHODS: Forty-two rats were randomly allocated to four groups as follows: controls: TPN and ENT, and TNF-infused: TPN + TNF and ENT + TNF. All groups received the same liquid defined formula diet either enterally or parenterally (isocaloric and isonitrogenous). Twenty-six rats were used for studies of body composition and metabolism and 16 for vascular permeability. RESULTS: TPN + TNF and ENT + TNF rats showed significantly increased liver weights and significantly reduced carcass weights compared with controls. A significant reduction in the muscle weights and total protein, as well as hyperglycemia, azotemia, and abnormal liver enzymes was also seen in ENT + TNF rats compared with ENT rats. The gastric and small intestinal mucosa was inflamed in the ENT + TNF but not in the ENT, TPN + TNF, and TPN rats. The plasma TNF levels determined by bioassay were significantly increased in the TPN + TNF and ENT + TNF rats compared with controls. There was increased vascular permeability in the stomach and small and large intestine in the ENT + TNF rats compared with ENT rats. No significant changes in vascular permeability were seen in TPN and TPN + TNF rats. CONCLUSIONS: ENT, but not TPN, resulted in prominent changes in the body composition and marked metabolic effects in the TNF-infused rats.

Animals↗
PubMedDate not supplied

Are patients fed appropriately according to their caloric requirements?

BACKGROUND: Specific morbidity related to underfeeding and overfeeding necessitates the design of nutrition support regimens that provide calories equal to those required on the basis of energy expenditure. This prospective multicenter trial was designed to determine what percent of patients in long-term acute care facilities receive feeding appropriate to their needs and whether accuracy of feeding has an impact on patient clinical status. METHODS: Patients on mechanical ventilation who were hospitalized at 32 Vencor Hospitals over a 9-week period and who were receiving only enteral nutrition by continuous infusion at a presumed goal rate were evaluated once by indirect calorimetry (IC) while on feeding. Caloric intake over the preceding 24 hours was determined by physician orders and by patient intake/output (I/O) record. Caloric requirements were defined by measured resting energy expenditure (REE) + 10% for activity. Degree of metabolism was defined by the ratio: (measured REE/Harris-Benedict predicted REE) x 100, and the degree of feeding by the ratio: (calories provided/calories required) x 100. RESULTS: IC was performed on 335 patients (mean, 11.2 patients per center; range, 1 to 32), of which 72 were excluded for nonphysiological results or failure to achieve steady state, 21 for receiving parenteral nutrition, and 29 for not being on mechanical ventilation at time of testing. The 213 study patients were 58.7% male with mean age 70.1 years (range, 20 to 90 years). Measured REE was <25 kcal/kg in 66.2% of patients and 25 to 35 kcal/kg in 28.6%. Barely half (48.4%) of this patient population was hypermetabolic. Based on physician orders, the majority of patients (58.2%) were overfed, receiving >110% of required calories, and 12.2% were underfed, receiving <90% of requirements. Discrepancies based on I/O records, however, suggested that 36.1% of patients received <90% of those calories ordered. By either basis, only about 25% of patients received feeding within 10% of required calories. The percent of patients being overfed varied between centers, ranging from 32.2% to 92.8%, and was not affected by years of facility IC experience or volume of IC studies per month. The pattern of caloric provision as measured by degree of feeding correlated inversely to degree of metabolism (p < .0001, R2 = .24). Accuracy of feeding had an impact on ventilatory status, as degree of feeding correlated inversely with minute ventilation (p = .001, R2 = .05). Degree of overfeeding also led to significant increases in azotemia (p = .033, R2 = .02). Extrapolating study data over 1 year, reduction in excess volume of enteral formula would have resulted in a cost savings of up to $1.3 million for the Vencor system. CONCLUSIONS: Because energy expenditure is difficult to predict on the basis of conventional equations, patients in long-term acute care facilities routinely are overfed and underfed, with only 25% receiving calories within 10% of required needs. Measuring a patient's energy requirement at least once by IC is important, because the degree of metabolism predicts how easily a patient will be underfed or overfed. The amount of infused calories should be compared with caloric requirements measured by IC, because the accuracy or degree of underfeeding or overfeeding has an impact on ventilatory status and the likelihood for developing azotemia. Although physician practice or bias may reduce the optimal clinical effect, the use of IC to determine caloric requirements may result in significant cost savings.

Adult↗
PubMed1986

Cumulative or delayed nephrotoxicity after cisplatin (DDP) treatment.

The present retrospective study reports data regarding renal toxicity in 115 patients (63 males, 52 females; median age, 56 years) who received cumulative doses of cisplatin (DDP) greater than or equal to 200 mg/m2. DDP was administered alone or in combination at a dose of 50-70 mg/m2 in 91 patients, and at a dose of 100 mg/m2 in 22 patients. Two patients after progression of ovarian carcinoma treated with conventional doses of DDP received 4 and 2 courses, respectively, of high-dose DDP (40 mg/m2 for 5 days) in hypertonic saline. The median number of DDP courses was 6 (range 2-14), and the median cumulative dose was 350 mg/m2 (range, 200-1200). Serum creatinine and urea nitrogen were determined before initiating the treatment and again 13-16 days after each administration. The incidence of azotemia (creatinina levels that exceeded 1.5 mg/dl) was similar before (7.8%) and after (6.1%) DDP doses of 200 mg/m2. Azotemia appears to be related to the association of DDP with other potentially nephrotoxic antineoplastic drugs (methotrexate) more than to the dose per course of DDP. Of 59 patients followed for 2 months or more after discontinuing the DDP treatment, 3 (5.1%) presented creatinine values higher than 1.5 mg/dl. The data deny that the incidence of nephrotoxicity is higher in patients receiving higher cumulative doses of DDP and confirm that increases in serum creatinine levels may occur some time after discontinuation of the drug.

Adolescent↗
PubMed2001

Predisposing factors for delirium in the surgical intensive care unit.

BACKGROUND: Delirium is a sign of deterioration in the homeostasis and physical status of the patient. The objective of our study was to investigate the predisposing factors for delirium in a surgical intensive care unit (ICU) setting. METHOD: Between January 1996 and 1997, we screened prospectively 818 patients who were consecutive applicants to the general surgery service of Dicle-University Hospital and had been kept in the ICU for delirium. All patients were hospitalized either for elective or emergency services and were treated either with medication and/or surgery. Suspected cases of delirium were identified during daily interviews. The patients who had changes in the status of consciousness (n = 150) were consulted with an experienced consultation-liaison psychiatrist. The diagnosis of delirium was based on Diagnostic and Statistical Manual of Mental Disorders (revised third edition) criteria and established through psychiatric interviews. Patients were divided into two groups: the "delirious group" (DG) (n = 90) and the "non-delirious group" (NDG) (n = 728). During delirium, all abnormal findings related to physical conditions, laboratory features, and additional diseases were evaluated as probable risk factors of delirium. RESULTS: Of 818 patients, 386 (47.2%) were male and 432 (52.8%) were female. Delirium developed in 90 of 818 patients (11%). The cases of delirium in the DG were more frequent among male patients (63.3%) than female patients (36.7%) (chi2 = 10.5, P = 0.001). The mean age was 48.9 +/- 18.1 and 38.5 +/- 13.8 years in the DG and NDG, respectively (t = 6.4, P = 0.000). Frequency of delirium is higher in the patients admitted to the Emergency Department (chi2 = 43.6, P = 0.000). The rate of postoperative delirium was 10.9%, but there was no statistical difference related to operations between the DG and NDG (chi2 = 0.13, P = 0.71). The length of stay in the ICU was 10.7 +/- 13.9 and 5.6 +/- 2.9 days in the DG and NDG, respectively (t = 0.11, P = 0.000). The length of stay in hospital was 15.6 +/- 16.5 and 8.1 +/- 2.7 days in the DG and NDG, respectively (t = 11.08, P = 0.000). Logistic regression was used to explore the associations between probable risk factors and delirium. Delirium was not correlated with conditions such as hypertension, hypo/hyperpotassemia, hypernatremia, hypoalbuminemia, hypo/hyperglycemia, cardiac disease, emergency admission, age, length of stay in the ICU, length of stay in hospital, and gender. It was determined that conditions such as respiratory diseases (odds ratio [OR] = 30.6, 95% confidence interval [CI] = 9.5-98.4), infections (OR = 18.0, 95% CI = 3.5-90.8), fever (OR = 14.3, 95% CI = 4.1-49.3), anemia (OR = 5.4, 95% CI = 1.6-17.8), hypotension (OR = 19.8, 95% CI = 5.3-74.3), hypocalcemia (OR = 30.9, 95% CI = 5.8-163.2), hyponatremia (OR = 8.2, 95% CI = 2.5-26.4), azotemia (OR = 4.6, 95% CI = 1.4-15.6), elevated liver enzymes (OR = 6.3, 95% CI = 1.2-32.2), hyperamylasemia (OR = 43.4, 95% CI = 4.2-442.7), hyperbilirubinemia (OR = 8.7, 95% CI = 2.0-37.7) and metabolic acidosis (OR = 4.5, 95% CI = 1.1-17.7) were predicting factors for delirium. CONCLUSION: We determined that conditions such as respiratory diseases, infections, fever, anemia, hypotension, hypocalcemia, hyponatremia, azotemia, elevated liver enzymes, hyperamylasemia, hyperbilirubinemia and metabolic acidosis were predicting factors for delirium.

Adult↗
PubMed2001

Antioxidants suppress mortality in the female NZB x NZW F1 mouse model of systemic lupus erythematosus (SLE).

Inflammation produces reactive oxygen intermediates (ROI) that cause vascular damage and activate T lymphocytes. Conversely, antioxidants not only protect tissue from oxidative damage but also suppress immune reactivity. The objective of this study was to examine immunomodulatory effects of the non-enzymatic antioxidants, N-acetylcysteine (NAC) and cysteamine (CYST), on autoimmune disease, glomerulonephritis, and mortality in the female B/W mouse model of human systemic lupus erythematosus (SLE). The development of murine lupus was assessed during the lifespan of female B/W mice given NAC or CYST. Morbidity and mortality were assessed daily. At 6 week intervals mice were examined for weight change, albuminuria, serum BUN, antibodies to DNA, and IgG immunoglobulin levels. Serum prolactin, estrogen and progesterone were measured at 18 weeks of age. In a parallel study, NAC- and CYST-treated and control B/W mice were examined at 24 weeks of age for interval renal histopathology, lymphocyte adhesion molecule expression, and antibody titers and in vitro cytokine production in response to immunization with DNP-KLH. CYST significantly suppressed development of albuminuria and azotemia at 36 and 42 weeks of age compared to control and NAC-treated mice. NAC significantly suppressed anti-DNA antibody levels at 24 weeks. In contrast CYST significantly increased anti-DNA antibody levels at 18 weeks of age (P < 0.001 CYST vs control and NAC-treated mice). Kidneys of CYST-treated mice also had accelerated inflammatory histologic changes despite their lower incidence of albuminuria and azotemia. Mean (+/- s.e.m.) survival of control mice was 33 +/- 2 weeks compared to 38 +/- 2 weeks in NAC-treated mice (P < 0.05 vs control), and 48 +/- 2 weeks in the CYST-treated group (P < 0.01 vs control mice). The antioxidants, NAC and CYST, significantly improved mortality in the female B/W mouse model of SLE. NAC suppressed autoantibody formation and modestly prolonged survival. CYST, despite its augmentation of anti-DNA levels and renal inflammatory changes, inhibited the development of renal insufficiency and markedly improved survival. These findings suggest that ROIs play a role in the pathogenesis of lupus nephritis and that antioxidants reduce the damage causing renal insufficiency. Antioxidants may be a beneficial adjunctive therapy in the treatment of human SLE.

Acetylcysteine↗
PubMed1988

Effects of interleukin-2 immunotherapy on renal function.

Recombinant interleukin-2 (IL-2) infusions have recently been evaluated as a new form of immunotherapy for the treatment of malignancies. This form of therapy has been complicated by the development of fluid retention, azotemia, and hypophosphatemia. To evaluate the effects of IL-2 on renal function, we prospectively studied eight patients who received IL-2 (10(5) micron/kg every eight hours intravenously [IV]) for five days as the initial phase of a treatment protocol using IL-2 plus lymphokine activated killer (LAK) cells. Dopamine and fluids were used to maintain blood pressure and all patients received indomethacin (100 mg/d). IL-2 therapy produced a syndrome similar to endotoxemia with the development of respiratory alkalosis (pH = 7.44 +/- .2, pCO2 = 30 +/- 2) and hypotension (mean BP, 71.3 mm Hg). These changes were accompanied by marked sodium avidity, edema formation, and mild elevations of BUN and creatinine. Hypophosphatemia, hypocalcemia, and hypomagnesemia were commonly seen. No defects in renal calcium, magnesium, phosphorous, net acid excretion, or glycosuria were demonstrated. We conclude: (1) IL-2 induces an increase in vascular permeability causing the development of edema, sodium avidity, and prerenal azotemia as occurs during endotoxemia; (2) IL-2 therapy induces respiratory alkalosis with the subsequent intracellular shift of phosphorous accompanied by increased renal phosphorous reabsorption; and (3) there is no evidence of renal tubular dysfunction (renal tubular acidosis [RTA], renal leak of glucose, phosphorous, or magnesium).

Acid-Base Equilibrium↗
PubMed1989

Phase II trial of outpatient interleukin-2 in malignant lymphoma, chronic lymphocytic leukemia, and selected solid tumors.

High-dose interleukin-2 (IL-2) with or without lymphokine-activated killer (LAK) cells has been reported to have activity in certain solid tumors, but toxicity has usually required hospitalization for administration. The purpose of this trial was to determine the antineoplastic effect and toxicity of IL-2 administered at a lower dose in an outpatient setting. Eligibility criteria included measurable disease, Karnofsky performance greater than or equal to 70%, age greater than 18 years, and adequate bone marrow, renal, and hepatic function. The median age of 35 patients was 56 years (range, 20 to 75). Diagnoses included malignant lymphoma (ML), (nine patients), chronic lymphocytic leukemia (CLL) (eight), melanoma (eight), colorectal cancer (six), renal cancer (two), and breast cancer (two). The initial 18 patients were treated with 1 mg/m2 (3 x 10(6) U/m2 intravenous [IV] bolus) for five days every other week for a total of 4 treatment weeks (8 weeks total). The subsequent 17 patients were treated with 0.5 mg/m2 (1.5 x 10(6) U/m2). All patients were evaluable for toxicity, and 26 for tumor response. Toxicities included fatigue (71%), nausea (69%), hypotension (54%), fever (51%), chills (40%), weight gain (37%), pruritus or rash (31%), dyspnea (14%), azotemia (6%), confusion (6%), thrombocytopenia (6%), and myocardial infarction (3%). Four patients died from apparently unrelated causes within the first 2 weeks of treatment. Treatment was discontinued before the completion of 8 weeks of treatment because of progressive disease (12 patients), severe hypotension (three), azotemia (one), myocardial infarction (one), early death (four), and miscellaneous causes (two). IL-2 at 1 mg/m2 IV for five days is associated with moderate toxicity, but a dose of 0.5 mg/m2 is tolerable for outpatient administration. Three partial responses (PR) and one minor response (MR) lasting 1 to 17+ months have been observed in 12 patients with ML and CLL evaluable for response. One additional MR was observed in a patient with melanoma. IL-2 deserves further study in patients with ML and CLL.

Adult↗
PubMed1990

Acute renal dysfunction during interleukin-2 treatment: suggestion of an intrinsic renal lesion.

Adoptive immunotherapy with interleukin-2 (IL-2) and lymphokine-activated killer (LAK) cells has been effective in treating some advanced malignancies in animals and humans. One complication of this treatment is a reversible, oliguric, acute renal failure, which has been ascribed to renal hypoperfusion and resultant prerenal azotemia. We serially studied renal function in 10 patients receiving high-dose regimens of recombinant interleukin-2 (rIL-2) to attempt to delineate further the nature of the renal dysfunction caused by IL-2 treatment. Renal plasma flow was computed from iodine 131 (I-131 Hippuran; Mediphysics, Paramus, NJ) orthoiodohippurate, excretion curves, and glomerular filtration rate (GFR) was determined by creatinine clearance. Studies done prior to and on day 4 of treatment showed that GFR fell in nine of 10 patients, with a mean decrease of 43% +/- 8%, and renal plasma flow fell in five of the 10 patients with a mean decrease of 5% +/- 10%. The average pretherapy filtration fraction was calculated to be 23% +/- 1% and after 4 days of treatment, decreased to a mean value of 15 +/- 2%. The BUN to creatinine ratio also declined in all patients. These findings collectively suggest that IL-2 nephrotoxicity may result from an intrarenal defect in addition to the previously described prerenal azotemia. Additionally, radionuclide studies of renal function are a reliable and reproducible noninvasive method of assessing these changes in renal function.

Acute Kidney Injury↗
PubMed1986

Subnormal concentrations of urinary epidermal growth factor in patients with kidney disease.

We determined the concentrations of immunoreactive epidermal growth factor (irEGF) and creatinine in urine samples from 47 adult patients with various kidney diseases and wide ranges of azotemia and proteinuria. In most of the patients, urinary irEGF concentrations (nanograms per mg creatinine) were markedly subnormal. In the entire group, urinary irEGF correlated with creatinine clearance (r = 0.79; P less than 0.001) and serum creatinine concentration (r = -0.85; P less than 0.001). In the subgroups of patients with primarily glomerular or tubulointerstitial diseases, similar correlations were found. By contrast, there was no correlation with proteinuria. We also determined the concentrations of plasma irEGF in five patients with azotemia. In four patients, the irEGF to creatinine concentration ratio was 1.9- to 8.9-fold higher in urine than in plasma, indicating that plasma irEGF was not the main source of urinary irEGF in these patients. Our data are compatible with the theory that urinary irEGF originates from nephrons per se.

Adolescent↗
PubMed1997

A control of a golden retriever with renal dysplasia.

A six-month-old male Golden Retriever with a three-month history of polyuria and polydipsia was examined. Hematological examinations revealed nonregenerative anemia, azotemia, high serum creatinine level, hypercalcemia, hyperphosphatemia, hypercholesterolemia, hyperamylasemia, and low level of total serum protein. Urinalysis indicated mild proteinuria, and low specific gravity. Radiographic and ultrasonographic examinations revealed bilateral small sized kidneys. Histological examination by renal biopsy confirmed the diagnosis of renal dysplasia. Treatment with a dietary protein restriction, oral adsorbents, and dried aluminum hydroxide gel have been performed in this dog, and then, azotemia, high serum creatinine level, hypercalcemia, and hyperphosphatemia were improved. During 10 months after the initiation of treatments, no significant clinical change except polydipsia and polyuria has been observed.

Animals↗
PubMed2005

Drug-induced nephropathy: an update.

Medications cause renal disease by promoting various types of injury in the kidney. Several drugs reduce renal perfusion and cause prerenal azotemia. Vascular disease can develop following exposure to various medications through direct and indirect effects. A number of glomerular lesions have been described with therapeutic agents and illicit drugs. Acute interstitial nephritis occurs from a drug-induced allergic reaction, which promotes interstitial inflammation and tubular damage. Acute tubular necrosis is a dose-dependent process that occurs from direct drug toxicity on tubular epithelia. Other less common patterns of drug-induced tubular injury include osmotic nephropathy, crystal nephropathy and acute nephrocalcinosis. Finally, postrenal azotemia from structural or functional obstruction of the urinary tract also complicates therapy with a number of medications.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

A hereditary model of slowly progressive polycystic kidney disease in the mouse.

There are two known forms of hereditary polycystic kidney disease (PKD) in humans. Although both forms initiate early in life, autosomal recessive PKD is rapidly progressive to kidney failure shortly after birth whereas autosomal dominant PKD is slowly progressive, taking many years to end stage. Research in this field has been limited by the availability of suitable animal models of PKD. Recently the C57BL/6J-cpk mouse has been used to study the pathogenesis of rapidly progressive hereditary PKD. The study presented here describes a slowly progressive PKD in the DBA/2-pcy mouse. The disease trait is transmitted in an autosomal recessive pattern and was localized to chromosome 9 through linkage to the dilute coat color and transferrin genes. Whereas some cystic changes were seen in fetal and newborn affected mice, renal enlargement did not develop until after 8 weeks of age and azotemia did not develop until after 18 weeks of age. Renal cysts were identified in all segments of the nephron and collecting duct and progressively enlarged with age. Individual cysts were found to be lined by a single layer of epithelial cells in most areas, with focal polyps and mounds of cells principally in collecting duct cysts. Early stages of cyst formation were associated with some abnormalities of tubular and glomerular basement membranes and accelerated eruption of incisors. Late stages of the disease were characterized by azotemia and chronic renal interstitial inflammatory infiltrates in all affected animals and cerebral vascular aneurysms in a few. We conclude that the DBA/2-pcy mouse has a form of renal cystic disease that appears similar in many respects to that seen in the dominant form of human PKD.

Animals↗
PubMed1994

Renal cancer complicating acquired cystic kidney disease.

Acquired cystic kidney disease (ACKD) occurs in the setting of prolonged azotemia and is therefore common in dialysis patients. It is characterized by epithelial proliferation, and its major complication is the development of renal cancer. The incidence of renal cancer is significantly increased in ACKD patients and is probably increased overall in the ESRD population as well. Those ESRD patients with suspicious symptoms, prolonged predialysis azotemia, or a dialysis duration of longer than 3 yr, or those who are candidates for a renal transplant should be screened for ACKD. Sonography or computed tomographic scanning are useful as initial screening tools. However, although more expensive and requiring contrast administration, the contrast-enhanced computed tomographic scan is the definitive imaging procedure by which to initially evaluate a renal mass. A suspicious renal mass is a patient who is a surgical candidate is an indication for a radical nephrectomy.

Carcinoma, Papillary↗