Effect of spironolactone on cisplatin-induced nephrotoxicity in rabbits.

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.

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.

Renal AA amyloidosis in a dairy cow in Turkey

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.

To determine whether patients with acute myocardial infarction undergoing thrombolysis with streptokinase develop changes in renal function. Prospective assessment of renal function in 60 consecutive patients admitted with acute myocardial infarction. Tertiary referral centre and city general hospital. 60 consecutive patients with acute myocardial infarction. Thirty eight were given streptokinase and 17 tissue plasminogen activator (alteplase) and five no thrombolytic agent (non-streptokinase group). Proteinuria and creatinine clearance on admission (day 1) and on days 3 and 6; serum urea and creatinine concentrations on days 1 and 7; streptokinase IgG on days 1, 2, and 7. Significant proteinuria (> 0.15 g/24 h) was found in 31 (82%) of the 38 patients in the streptokinase group (mean 0.47 g/24 h (95% confidence interval 0.35 to 0.6 g/24 h)) in the 24 hours after admission compared with six (27%) out of 22 in the non-streptokinase group (mean 0.17 g/24 h (0.12 to 0.2 g/24 h); P = 0.008). In the streptokinase group this decreased to the normal range by day 3 (mean 0.15 g/24 h (0.1 to 0.22 g/24 h); P = 0.0001 v baseline). Electrophoresis of urine showed the proteinuria to be glomerular in origin. Creatinine clearance and serum creatinine and urea concentrations were similar in both groups. In the streptokinase group detectable streptokinase IgG titres were found in 28 out of 32 (87%) patients. The median titre on admission was 16 (range 0-110); it fell to 3 (range 0-80; P = 0.001) by day 2 and increased to 61 (range 0-7700; P = 0.0002 v baseline) by day 7. Streptokinase was associated with significant early onset proteinuria of glomerular origin. This started to resolve by day 3 and resulted in no deterioration in overall renal function. The temporal relation to the initial fall in antibody titre suggests that it could be the result of immune complex deposition in the glomeruli.

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.

Tyrimo tiklas išsiaiškinti bendrinės anestezijos su aukšta epidūrine analgezija (TEA) ir bendrinės anestezijos (BA) poveikį inkstų funkcijai po vainikinių jungčių suformavimo (VAJO) operacijos, dirbtinės kraujo apytakos (DKA) sąlygomis. Medžiaga ir metodai. Į tyrimą įtraukti pacientai (49 - 82 metų), kuriems nuo 2014 m. spalio iki 2015 m. spalio LSMUL KK Širdies, krūtinės ir kraujagyslių chirurgijos klinikoje buvo atliekamos VAJO DKA sąlygomis. Pacientai buvo suskirstyti į dvi grupes: BA, jai priklausė pacientai, kuriems taikyta tik bendrinė anestezija (inhaliuojamieji anestetikai ir i/v opiatai); ir TEA (vietinis anestetikas ir BA inhaliuojamieji anestetikai su i/v opiatais) grupę, jai priklausė pacientai, kuriems operacijos metu taikyta aukšta krūtininė epidūrinė anestezija, kombinuota su bendrine anestezija. Tiriamiesiems pacientams tris kartus buvo daromas biocheminis kraujo tyrimas – prieš operaciją, pirmą parą po operacijos, penktą parą po operacijos. Vertintos kreatinino ir šlapalo koncentracijos kraujo serume perioperaciniu laikotarpiu, kurios atspindi inkstų funkcijos sutrikimą [2]. Atlikto tyrimo rezultatai. Įvertinus prieš operaciją kreatinino koncentraciją TEA grupėje vidurkis buvo 93,3 ±16 mmol/l, BA grupėje - 95,3 ±23,5 mmol/l (p&gt;0,05). Pirmą parą po operacijos kreatinino vidurkis TEA grupėje buvo 101,3 ±19,3 mmol/l , BA grupėje - 104,81 ±37 mmol/l.(p&amp;lt;0,05). Penktąją parą TEA grupėje kreatinino koncentracija buvo 97 ±14,3mmol/l, o BA grupėje - 103,7 ±31,6 mmol/l. (p&amp;lt;0,05). Įvertinus prieš operaciją šlapalo koncentraciją TEA grupėje vidurkis buvo 4,2±1,19 mmol/l, BA grupėje 5,2 ±1,7 mmol/l (p&gt;0,05). Pirmą parą po operacijos šlapalo vidurkis TEA grupėje 5,6±1,8 mmol/l,BA grupėje 6,2 ±2,0 mmol/l.(p&gt;0,05). Penktąją parą TEA 4,7 ±1,3 mmol/l , o BA 5,8 ±3 mmol/l (p&amp;lt;0,05). Tyrimo išvados. Palyginus abiejų grupių rodiklius, TEA grupėje pastebimas mažesnis kreatinino ir šlapalo koncentracijų kitimas, lyginant koncentracijas prieš operaciją, viena diena po ir penkios dienos po operacijos nei BA grupėje.

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.

In this study, the in vivo hypoglycemic effect of a donut-shaped polyanion salt (NH4)14[Na@P5W30O110]·31H2O {NaP5W30} and its Ag-containing derivative K14[Ag@P5W30O110]·22H2O·6KCl {AgP5W30}, as well as their hepatotoxicity and nephrotoxicity, was evaluated. In the screening hypoglycemic study, Wistar albino rats with streptozotocin induced diabetes were treated intraperitoneally with three single doses (5, 10, and 20 mg per kg per b.w.) of both investigated polyoxotungstates. The blood glucose levels, measured before and after 2, 4 and 6 h polyoxotungstate application, showed that both studied compounds induced the most pronounced and time dependent glucose lowering effects at the doses of 20 mg kg−1. Thus, daily doses of 20 mg kg−1 were administered to Wistar albino rats orally for 14 days in further toxicity examinations. The serum glucose concentration and biochemical parameters of kidney and liver function, as well as a histopathological analysis of kidney and liver tissues were evaluated 14 days after the polyoxotungstate administration. Both investigated compounds did not induce statistically significant alterations of the serum glucose and uric acid concentrations, as well as some of the liver function markers (serum alanine and aspartate aminotransferases, and alkaline phosphatase activities). However, the significant decrease in serum total protein and albumin concentrations and the increase in biochemical parameters of renal function – serum urea (up to 63.1%) and creatinine concentrations (up to 23.3%) were observed for both polyoxotungstates. In addition, the detected biochemical changes were in accordance with kidney and liver histhopathological analysis. Accordingly, the hepatotoxic and nephrotoxic effects of these potential antidiabetic polyoxotungstates could be considered as mild.

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.

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.

Ethnopharmacological relevance: Pistacia integerrima J.L. Stewart ex Brandis (Family Anacardiaceae) galls are used in Indian ethnomedicine for their antiasthmatic, antioxidant anti-inflammatory, sedative, and spasmolytic properties. However, no scientific studies demonstrate its nephroprotective potential against Cisplatin-induced nephrotoxicity. Materials and Methods: The effect of the essential oil of Pistacia integerrima (7.5, 15 and 30 mg/kg/day) and standard drug Vitamin E (250 mg/kg/day) on the kidney was examined 5 days after treatment with Cisplatin (12 mg/kg body weight, i.p.) induced oxidative renal damage in mice. Renal injury was assessed by assessment of serum creatinine and blood urea nitrogen. Renal oxidative stress was estimated by renal malondialdehyde levels, reduced glutathione levels and enzymatic activities of superoxide dismutase and catalase. Results: Essential oil of Pistacia integerrima (7.5, 15 and 30 mg/kg/day) significantly (p &lt; 0.001) protected the nephrotoxicity induced by Cisplatin. The Cisplatin-induced increase in serum urea and creatinine concentrations was reduced in the essential oil of Pistacia integerrima treated groups. Essential oil of Pistacia integerrima treatment also increased the Cisplatin-induced decline of renal antioxidant enzymes such as superoxide dismutase, catalase, and Glutathione activities. Essential oil of Pistacia integerrima increased the concentration of reduced glutathione and protected the increase of Cisplatin-induced lipid peroxidation. Histopathological investigations of the kidney showed a protective effect of the essential oil of Pistacia integerrima in mice. The essential oil of Pistacia integerrima was found to be effective in protecting against oxidative renal damage. The protection is mediated by preventing the decline of renal antioxidant status. Conclusion: The present investigation demonstrates that the essential oil of Pistacia integerrima Stewart ex Brandis has a protective effect on cisplatin-induced experimental nephrotoxicity, and this effect is attributed to its direct anti-inflammatory and strong antioxidant profile. Hence, the essential oil of Pistacia integerrima Stewart ex Brandis has a solid potential to be used as a therapeutic adjuvant in cisplatin nephrotoxicity.

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.

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.