Renal AA amyloidosis in a dairy cow in Turkey

Acetaminophen overdose may be accompanied by electrolyte disturbances. The basis for electrolyte change appears to be due to increased fractional urinary electrolyte excretion. This study investigated the impact of serum acetaminophen concentration on changes in serum potassium, creatinine and urea concentrations in patients with acetaminophen overdose. This was a retrospective cohort study which included patients admitted to the emergency department and hospital within 24 h of acetaminophen ingestion. The study was conducted over a period of 5 years from 1 January 2004 to 31 December 2008. Data are presented as mean ± SD and as medians (interquartile range) and groups were compared using independent two-tailed Student t-test. Statistical Package for Social Sciences (SPSS) 15 was used for data analysis. Two hundred and eighty-three patients were studied (44 males and 239 females), mean age 23 ± 7.5 years. Patients who had a serum acetaminophen concentration above a 'possible toxicity' treatment line were associated with an elevation in serum creatinine concentration (p=0.044) and a reduction in the serum potassium concentration (p<0.001) but were not associated with a reduction in serum urea concentration (p>0.99). During the study period, 63.3% (179 patients) had serum potassium concentrations less than the normal concentration (3.5 mmol/l) and 31.4% (89 patients) had serum urea concentrations less than the normal concentration (2.5 mmol/l). The serum creatinine concentration in all patients was within the normal range. Acetaminophen appears to cause a concentration-dependent reduction of potassium concentrations and an elevation of creatinine concentrations of short duration (<24 h) after overdose.

Summary To evaluate the effects of compensated heart failure (hf) on digoxin pharmacokinetic properties in cats, 6 cats with dilated cardiomyopathy were compared with 6 clinically normal (control) cats. Digoxin tablets were administered at a dosage of 0.01 mg/kg of body weight, q 48 h for approximately 10 days, until presumed steady state was reached. Both groups were treated concomitantly with aspirin, furosemide, and a commercial low-salt diet. Retrospectively, control and hf cats were calculated to be at 95% and 97% steady state, respectively. At the time blood samples were collected, hf cats were clinically compensated. Serum digoxin concentration ([dxn]) was determined by radioimmunoassay on samples drawn immediately before and 1, 2, 4, 8, 12, 24, 34, and 48 hours after digoxin administration. Measured and calculated values (peak, 8-hour, and mean [dxn]; elimination half-life [t½]; oral clearance; and hours during which [dxn] was in the toxic range) were not significantly different between control and hf cats. To predict individual propensity for digoxin intoxication serum creatinine and urea concentrations and sulfobromophthalein dye retention were measured in control and hf cats prior to the onset of treatment with digoxin. There was no statistically significant correlation between serum creatinine and urea concentrations when compared with sulfobromophthalein dye retention nor between any of these values and digoxin peak, 8-hour, and mean concentrations or t½, oral clearance, or hours during which [dxn] was in the toxic range. Mean serum creatinine and urea nitrogen concentrations were significantly greater (P &lt; 0.01) and sulfobromophthalein dye retention approached significant prolongation (P &lt; 0.06) in hf cats, compared with that in control cats. All hf cats with sulfobromophthalein dye retention &gt; 5% at 30 minutes became digoxtn-intox-icated, on the basis of [dxn]; no hf cats with normal sulfobromophthalein dye retention became intoxicated. In compensated heart failure, digoxin pharmacokinetic properties are not altered beyond that expected when concurrent antithrombotic and offloading treatments with aspirin, furosemide, and commercial low-saltdiet are used. In addition, digoxin treatment q 48 h produces adequate serum concentrations in the cat, with steady state being reached after approximately 10 days of digoxin treatment in hf cats given concomitant treatment. Digoxin toxicosis can be expected in approximately 50% of animals given digoxin tablets at a dosage of 0.01 mg/kg, q 48 h, with the additional treatment described. Because of individual variation, [dxn] should be monitored to minimize digoxin toxicity and maximize its therapeutic efficacy. Blood samplings 8 hours after digoxin administration, after attaining approximate steady-state conditions in the animal, is recommended. Although serum urea and creatinine concentrations and sulfobromophthalein dye retention did not predict digoxin pharmacokinetic properties, the latter test may be useful in determining which cats will become digoxin-intoxicated.

BackgroundAcute kidney injury (AKI) is frequent among critically ill patients. Renal replacement therapy (RRT) is often required to deal with severe complications of AKI. This technique is however associated with side effects such as hemodynamic instability and delayed renal recovery. In this study, we aimed to describe a novel model of hemodialysis in rats with AKI and depict a dialysis membrane performance.MethodsEighteen Sprague–Dawley rats received 0.75% adenine-rich diet to induce AKI. After 2 weeks, nine underwent an arterio-venous extracorporeal circulation (ECC) (ECC group) for 2 h without a dialysis membrane on the circuit and nine received a hemodialysis session (HD group) for 2 h with an ECC circuit. All rats were hemodynamically monitored, and glomerular filtration rate (GFR) was measured by transcutaneous fluorescence after the injection of FITC-Sinistrin. Blood samples were collected at different time points to assess serum creatinine and serum urea concentrations and to determine the Kt/V. Sinistrin concentration was also quantified in both plasma and dialysis effluent.ResultsAfter 2 weeks of adenine-rich diet, rats exhibited a decrease in GFR. Both serum urea and serum creatinine concentrations increased in the ECC group but remained stable in the HD group. We found no significant difference in serum creatinine and serum urea concentrations between groups. At the end of experiments, mean serum urea was 36.7 mmol/l (95%CI 19.7–46.9 mmol/l) and 23.6 mmol/l (95%CI 15.2–33.5 mmol/l) in the ECC and HD groups, respectively (p = 0.15), and mean serum creatinine concentration was 158.0 µmol/l (95%CI 108.1–191.9 µmol/l) and 114.0 µmol/l (95%CI 90.2–140.9 µmol/l) in the ECC and HD groups, respectively (p = 0.11). The Kt/V of the model was estimated at 0.23. Sinistrin quantity in the ultrafiltrate raised steadily during the dialysis session. After 2 h, the median quantity was 149.2 µg (95% CI 99.7–250.3 µg).ConclusionsThis hemodialysis model is an acceptable compromise between the requirement of hemodynamic tolerance which implies reducing extracorporeal blood volume (using a small dialyzer) and the demonstration that diffusion of molecules through the membrane is achieved.

This study was designed to examine, the effect of Effective aqueous extract Lawsonia inermis leaves as antioxidant on concentration of Urea ,Criatinine and Histological of kidneys in Albino male Rats exposed to hydrogen peroxide induced oxidative stress. This study showed that 0.5% hydrogen peroxide concentration leds to significant increase (P&lt;0.05( in concentration of serum urea and creatinine comparing with control group. While the aqueous extract of Lawsonia inermis concentration (50mg/kg) led to significant decrease (P&lt;0.05) in concentration of serum urea and creatinine compare with control group. Also the results showed no significant increase in concentration of urea and creatinine in group exposed to oxidative stress and aqueous extract of Henna comparing with control group. The histological results of the kidney treated with (0.5%) H2o2 showed degeneration, congestion, lymphatic infilteration, vacuolation in the renal tubules with necrosis comparing with control. While sections of kidney treated with aqueous extract of Henna showed normal appearance of the renal tubules. Histological investigation of kidneys rats treated with H2O2 and extract of Henna showed improvement in histological picture with reduction in infilteration, vacuolation and necrosis but the tissue did not return back to the normal state.

Cystatin C is a serum protein with low molecular mass, which has been suggested as a marker to assess renal function in the dog. This protein is regularly assessed using particle-enhanced turbidimetric immunoassay (PETIA) and particle-enhanced nephelometric immunoassay (PENIA), in which rabbit anti-human cystatin C antibodies are used. The purpose of this work was to compare the results of cystatin C analysis obtained by PETIA and PENIA assays in the dog. Forty dogs of different genders and breeds were classified into four groups of 10 animals each based on serum creatinine concentrations (4 stages of chronic kidney disease). Serum cystatin C concentration was measured using PETIA and PENIA assays, the results were compared, and correlation with serum urea and creatinine concentrations was established. The correlation coefficient for results obtained using PETIA and PENIA assays was r = 0.706. Serum cystatin C concentrations obtained in PETIA had a lower correlation coefficient with creatinine concentrations than those found in PENIA (r = 0.614 and r = 0.904, respectively); similarly, serum cystatin C was less correlated with serum urea concentration in PETIA than in PENIA (r = 0.463 and r = 0.636, respectively). The results obtained in this study suggest that the nephelometric assay is more sensitive and was shown to be more closely correlated with other renal function indicators than the PETIA assay.

The purpose of the present study was to examine the protective effect of FK453, (+)-(R)-1-[(E)-3-(2-phenylpyrazolo [1,5-a] pyridin-3-yl) acryloyl]-2-piperidine ethanol, a potent non-xanthine (adenosine A1 receptor antagonist, on glycerol-induced acute renal failure (ARF) in rat in comparison with the effects of FR113452 (S-(-) enantiomer of FK453), 1,3-dipropyl-8-cyclopentyl-xanthine (adenosine A1 receptor antagonist), theophylline (nonselective adenosine receptor antagonist), CGS15943 [1,2,4] triazolo [1,5-C] quinazolone, adenosine A2A receptor antagonist), and typical diuretics (hydrochlorothiazide and furosemide). FK453 (1 and 10 mg/kg orally) significantly reduced serum creatinine and urea concentrations in 25% glycerol (10 ml/kg intramuscularly)-induced ARF by protective treatment. The effect was similar to that of 1,3-dipropyl-8-cyclopentyl-xanthine and theophylline. FR113452 and CGS15943 had little effect on serum creatinine and urea concentrations. In contrast, hydrochlorothiazide and furosemide increased serum creatinine and urea concentrations. FK453, hydrochlorothiazide, and furosemide did not have any effect on either serum creatinine or urea concentration in 25% glycerol-induced ARF by therapeutic treatment. In 50% glycerol (10 ml/kg im)-induced ARF, FK453 reduced serum creatinine and urea concentrations, and increased urine volume and creatinine clearance. The results of the present study showed that FK453, a potent nonxanthine adenosine A1 receptor antagonist, ameliorated glycerol-induced ARF in the rat. The findings support the idea that adenosine is an important factor in the development of glycerol-induced ARF in the rat and that the protective effect of adenosine receptor antagonist is mediated via the adenosine A1 receptor. Drug Dev. Res. 39:47–53 © 1997 Wiley-Liss, Inc.

The effects of co-administration of oral chloroquine with paracetamol or with ibuprofen on renal function were studied using 6 groups of New Zealand White rabbits. Group 1, the control group received only feed and water. The other groups (Groups 2-6) either received single therapies of paracetamol (10 mg/kg of body weight every 6 hours), ibuprofen (20 mg/kg of body weight/day) or chloroquine (5 mg/kg of body weight/day) or combined therapies of chloroquine and paracetamol or chloroquine and ibuprofen for 8 days. Measurements of serum urea, creatinine and electrolyte concentrations were used to assess renal function in these animals. The chloroquine-treated group had a significant (p<0.05) decrease in serum sodium and potassium concentrations and a significant increase (p<0.05) in serum urea and creatinine concentrations when compared with the corresponding values of the control group. The groups treated with combined therapy (groups 5 and 6) had significant increases (P<0.05) in serum urea and creatinine concentrations, and significant decreases in sodium and potassium levels when compared with the chloroquine-treated group (group 4). These results confirm that acute administration of chloroquine impairs kidney function and further shows that this renotoxicity is exacerbated when chloroquine is co-administered with paracetamol or with ibuprofen, two common drugs used to manage fever. Key words: Chloroquine, co-administration, paracetamol, ibuprofen renal toxicity.

As determinações de creatinina e uréia têm sido utilizadas para avaliar o impacto do treinamento físico. Portanto, o principal objetivo do presente estudo foi verificar o comportamento das concentrações séricas e urinárias de creatinina e uréia em futebolistas profissionais ao longo de uma periodização. Participaram do estudo 18 jogadores de futebol que foram avaliados no início (T1), meio (T2) e fim (T3) de uma periodização específica. Os atletas foram submetidos às avaliações antropométrica e de determinação da capacidade aeróbia e da eficiência do metabolismo anaeróbio alático. As concentrações de creatinina e uréia dos atletas foram mensuradas no soro e na urina, além da taxa de filtração glomerular (TFG), determinada por três métodos distintos, sendo um independente e dois dependentes do volume urinário. A análise das respostas das variáveis em T1, T2 e T3 foi realizada por Anova one-way, seguida de post hoc de Newman-Keuls, assim como foi aplicado teste de correlação de Pearson. Para todos os casos o nível de significância prefixado foi de 5%. Houve melhora nos parâmetros aeróbio (p &lt; 0,01) e anaeróbio alático (p &lt; 0,01) ao longo da periodização, assim como foi verificada diminuição do volume urinário (p &lt; 0,05) ao longo do estudo. As concentrações de creatinina apresentaram comportamento oposto quando determinadas no soro (p &lt; 0,05) e na urina (p &lt; 0,01) ao longo da periodização, não apresentando correlações significativas. Todos os métodos de determinação de TFG mostraram redução dos valores (p &lt; 0,05) em resposta ao treinamento periodizado. Foram observadas correlações significativas entre todos os métodos em T1, e também em T2 e T3 apenas entre os métodos dependentes do volume urinário. De acordo com os resultados, é possível concluir que as concentrações de creatinina determinadas no soro e na urina de futebolistas profissionais foram sensíveis ao programa de treinamento desenvolvido; contudo, apresentaram comportamentos opostos. Isso provavelmente ocorreu devido à limitação metodológica da técnica de coleta de urina de 24h.

Twenty-five male Wistar rats (140–170 g) were partitioned into 5 groups (n = 5). 2.5 mg/kg, 5 mg/kg, 10 mg/kg and 20 mg/kg of combine Tartrazine and Erythrosine (T+E; 50:50) were administered for 23 days. Serum urea and creatinine, gene expression and profiling of pro-inflammatory cytokine (Tumor Necrosis Factor- α gene), Caspase-9 and Kidney injury molecule-1 (KIM-1) and histomorphological examination of the kidney were investigated. The fold change of relative gene expression of TNF-α gene showed significantly (p < 0.05) up-regulation in all the treated rats except for the 10 mg/kg T+E treated rats when compared to control rats. Casp-9 and KIM-1 genes were significantly (p < 0.05) up-regulated in low dose treatment (2.5 mg/kg T+E and 5 mg/kg T+E) and down-regulated in high dose treatment (10 mg/kg T+E and 20 mg/kg T+E). However, there was significant (p < 0.05) increase in serum urea concentration in the rats treated with 5 mg/kg T+E and 20 mg/kg T+E while the rats treated with 10 mg/kg T+E indicated a significant (p < 0.05) decrease. Conversely, serum creatinine concentration indicated significant (p < 0.05) increase in10mg/kg T+E and 20 mg/kg T+E treated rats versus the control. From the histomorphological examination of the kidney, there was hypertrophy of the glomeruli in relation to the size of Bowman’s capsule in the 10 mg/kg T+E and 20 mg/kg T+E treated rats. Kidney function was impaired as evident in up-regulation of TNF-α gene, KIM-1 gene, and serum urea and creatinine concentration with down-regulation of Casp-9 gene. The combined treatment also tampers with the architecture of the kidney.

Emergency abdominal surgery carries considerable postoperative morbidity and mortality. Hypovolaemia is considered to be a cause of renal hypoperfusion, which is associated with a decreased clearance of serum urea and creatinine. This study examines whether the perioperative serum urea and creatinine concentrations are predictors of mortality in patients undergoing emergency abdominal surgery. Consecutive patients (n=300) who underwent emergency abdominal surgery were studied. Age- and sex-specific reference intervals were used for the data analysis. Patients with incomplete biochemical (n=51) or mortality data (n=31) or with pre-existing renal failure (n=9) were excluded from the analysis. 209 patients were analysed, of whom 162 (78%) remained alive and 47 (22%) died following surgery. The non-survivors were older (P<0.05), had undergone more extensive surgery (P<0.001) and were more likely to have been admitted to the intensive care unit (P<0.001). The serum urea concentration was higher preoperatively (P<0.05) and on day one postoperatively (P<0.001) in the non-survivors. On multivariate logistic regression analysis, age (odds ratio [OR] 3.27, 95% confidence interval [CI] 1.43-7.47, P<0.005), severity of surgery (OR 2.21, 95% CI 1.14-4.29, P<0.019), admission to intensive care (OR 0.54, 95% CI 0.11-0.54, P<0.001), seniority of anaesthetist (OR 0.50, 95% CI 0.27-0.90, P<0.022) and day one urea (OR 3.33, 95% CI 1.39-7.99, P<0.007) were independently associated with 30-day mortality. These results indicate that an increased serum urea concentration, but not serum creatinine concentration, in the postoperative period is associated with an increase in 30-day mortality in patients undergoing emergency abdominal surgery.

Brown Swiss (BS) cows have greater urea concentrations in milk and blood compared with Holstein (HO) cows. We tested the hypothesis that BS and HO cows differ in kidney function and nitrogen excretion. Blood, saliva, urine, and feces were sampled in 31 multiparous BS and 46 HO cows kept under identical feeding and management conditions. Samples were collected at different lactational stages after the monthly DHIA control test-day. To test the glomerular filtration rate (GFR) and urea excretion, concentrations of creatinine and urea were measured in serum, urine, and saliva. As an additional marker to estimate GFR, we determined symmetric dimethylarginine (SDMA) in serum. Feces were analyzed for dry matter content and nitrogen concentration. Data on milk urea and protein concentrations, and daily milk yield were obtained from the monthly DHIA test-day records. The effects of breed, time, and parity number on blood, saliva, urine, feces, and milk parameters were evaluated with the GLM procedure with breed, time, and parity number as fixed effects. Differences between BS and HO were assessed by the Tukey-corrected t-test at P < 0.05. Concentrations of urea, creatinine, and SDMA in serum, were greater in BS than in HO cows (P < 0.01): 5.46 ± 0.19 vs 4.72 ± 0.13 mmol/L (urea), 105.96 ± 2.23 vs 93.07 ± 1.50 mmol/l (creatinine), and 16.78 ± 0.69 vs 13.39 ± 0.44 µg/dL (SDMA). We observed a greater urea concentration in BS cows (25.8 ± 0.7 vs 21.8 ± 0.7 mg/dL) and protein content in milk (3.70 ± 0.08 vs 3.45 ± 0.07%) than in HO cows (P < 0.01). Urea and creatinine concentrations in urine and saliva did not differ among breeds. No differences between BS and HO were observed for milk yield, fecal DM, and fecal nitrogen content. Dry matter intake and body weight were similar in BS and HO cows (P > 0.05). Despite greater urea, creatinine, and SDMA concentrations in blood as well as a higher milk urea content in BS compared with HO, respective concentrations in urine did not differ between breeds. In conclusion, our results demonstrate a lower renal GFR in BS compared with HO cows, thereby contributing to the greater plasma urea concentration in BS cows. However, estimation of nitrogen excretion via milk, urine, and feces does not entirely reflect nitrogen turnover within the animal.

The interpretation of traditional serum urea and creatinine concentrations as indices of the severity of uremia requires major modifications in hemodialyzed patients. Although high urea concentrations usually signify worsening uremia and inadequate dialysis, low concentrations do not guarantee a good outcome. Urea production as modified by diet and other factors must also be included in a complete description of dialysis quantity and adequacy. The expression 'Kt/V' is a measure of hemodialysis that includes both urea removal and urea generation and is easy to measure from predialysis and postdialysis serum urea concentrations. Kt/V can be most precisely measured with the aid of mathematical models of urea kinetics during and between hemodialyses. Although a reliable measure of the dialysis dose received by most patients, the single-compartment model overestimates serum urea concentrations during hemodialysis and fails to predict the rebound immediately following dialysis. The classic two-compartment model that includes a factor for resistance to diffusion between the compartments, more accurately predicts the BUN profile but fails to account for blood flow-related disequilibrium including cardiopulmonary recirculation. Since solute disequilibrium reduces the effectiveness of hemodialysis, models that incorporate equilibrated urea concentrations both before and after hemodialysis are potentially more accurate tools for quantifying dialysis. Dialysate methods have the potential to accurately measure both solute removal which is the ultimate goal of dialysis, and patient clearance which is considered a better measure of the dialysis effect than dialyzer clearance. Application of these newer techniques requires major changes in sampling methods and changes in analytical equipment that will delay implementation. Meanwhile, analysis of blood-side urea concentrations using the single-compartment, variable volume model provides a reasonable estimate of Kt/V but must be interpreted with due consideration of its well-recognized pitfalls.

Background and objective: exposure to lead continues to a serious public problem. The objective is to elucidate the effect of lead acetate exposure on serum Concentration of urea and creatinine in adult female rats.Methods: Forty eight adults female rats divided in to four groups (12 rats/group) .Group 1, (T1) ,given date palm pollen (150 mg/kg. B.W.) Group 2,(T2) given lead acetate (10mg/kg. B.W.), group 3, (T3) given lead acetate (10mg/kg.B.W.) and date palm pollen (150 mg/kg. B.W) for 6 weeks, Group 4(Control) ,given distilled water. Serum concentration of urea and creatinine was evaluated via ELISA method for all groups.Results: The mean concentration of urea showed no significant difference between,(T1) and (T3) while in T2 a significant (p < o.o5) increase in urea concentration compared to T1&T3 . There was no significant difference within groups in urea concentration. Group (T1) exposed to DPP showed no significant decrease in serum creatinine on zero,14 , 28 day & 42 day post exposure respectively . Group (T2) exposed to lead acetate showed significant increase of creatinine concentration compared with control and (T1) group .Group (T3) showed significant decrease in creatinine levels compared with T2 group and these levels become closely to control group. Histological changes indicated that DPP significantly meliorate the toxic effects of lead acetate in glomeruli, collecting tubules associated with obvious decrease in inflammatory response.Conclusion: DPP has the ability to counteract the toxic effect of lead acetate associated with improvement of renal histology and serum concentration of urea and creatinine.

The clinical use of cisplatin is highly restricted, because of its nephrotoxicity. In this study the protective effect of Nigella sativa (N. sativa) against cisplatin-induced nephrotoxicity was investigated in rats. In the current study, the effects of the administration of aqueous-ethanolic extract of N. sativa (100 and 200 mg/kg, BW) and vitamin E (100 mg/kg, BW) against blood and urine biochemical alterations and kidney function in rats treated with cisplatin were investigated. Cisplatin was injected at a dose of 6 mg/kg, BW, on the sixth day of the experiment. The results indicated significant changes in serum urea and creatinine concentration, urine glucose concentration, and urine output in cisplatin group compared with control group. Serum urea and creatinine concentration in preventive and preventive+treatment vitamin E and preventive+treatment N. sativa (200 mg/kg, BW) groups and also serum creatinine concentration in preventive+treatment N. sativa (100 mg/kg, BW) group significantly decreased compared with cisplatin group. Urine glucose concentration in preventive and preventive+treatment N. sativa groups and urine output in preventive and preventive+treatment N. sativa (200 mg/kg, BW) groups significantly decreased compared with cisplatin group.Osmolarity excretion rate in preventive and preventive+treatment vitamin E and preventive N. sativa groups was significantly higher than control group. The current study suggests that N. sativa extract and vitamin E in a dose- and time-dependent manner improved the serum and urine biochemical parameters and kidney function in cisplatin-induced nephrotoxicity in rats. However, it needs more investigations to determine the mechanism of N. sativa action on cisplatin-induced kidney toxicity.

To assess the prevalence of renal abnormalities in ragdoll cats. Ragdoll breeders often warn clients to watch for future renal problems, mainly due to chronic interstitial nephritis and polycystic kidney disease. Therefore, ragdoll screening by abdominal ultrasonography, measurement of serum creatinine and urea concentrations and genetic testing is often performed without documented scientific evidence of increased risk of renal disease. Retrospective evaluation of ragdoll screening for renal disease at one institution over an eight-year period. Renal ultrasonography was performed in 244 healthy ragdoll cats. Seven cats were positive for polycystic kidney disease, 21 were suspected to have chronic kidney disease, 8 had abnormalities of unknown significance and 2 cats had only one visible kidney. Cats suspected to have chronic kidney disease were significantly older and had significantly higher serum urea and creatinine concentrations than cats with normal renal ultrasonography. All 125 genetically tested cats were negative for polycystic kidney disease. However, only one of the seven ultrasonographically positive cats underwent genetic testing for polycystic kidney disease. Ultrasonographic findings compatible with chronic kidney disease were observed in almost 10% of cats, and polycystic kidney disease occurred at a low prevalence (<3%) in this ragdoll population. Further studies are required to elucidate if ragdoll cats are predisposed to chronic kidney disease.