Protein-to-creatinine urinary in the early diagnosis of renal injury in canine pyometra

ABSTRACT: Kidney disease that affects bitches with pyometra may lead patients to develop chronic renal failure even after pyometra treatment. Therefore, several studies have sought to clarify the gaps in the understanding of the pathogenesis of renal injury in pyometra. Identification of early detection markers for renal damage, which can predict and identify the prognosis of the disease, is very important. Proteinuria analysis can diagnose kidney damage, since proteins such as albumin are not filtered through the glomerulus and those that undergo glomerular filtration are almost completely reabsorbed by tubular cells. The objective of this study was to evaluate whether the urinary protein-to-creatinine ratio (UPC) can detect renal injury in bitches with pyometra before development of azotemia. For this, 44 bitches with pyometra were divided into two groups: bitches with azotemic piometra (A, n=15, creatinine >1.7) and bitches with non-azotemic pyometra (NA, n=29). The two groups were compared to the control group (CG, n=12), which had no signs of systemic disease. All animals underwent blood and urine tests. Leukocytosis was more evident in bitches in the A group than in the other groups. This shows that the inflammatory response may be associated with the pathogenesis of renal injury. The median UPC in bitches with pyometra was significantly higher than in the CG, with a median above the reference values. In conclusion, the UPC can be used in bitches with pyometra to detect renal damage before the development of azotemia. It has been suggested that the UPC of bitches with pyometra should be followed through during the postoperative period so that permanent renal lesions secondary to pyometra can be diagnosed and treated properly before the development of azotemia.

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Using Transgenic Mice to Analyze the Mechanisms of Progression of Chronic Renal Failure

Journal of the American Society of Nephrology ◽

10.1681/asn.v11suppl_2s144 ◽

2000 ◽

Vol 11 (suppl 2) ◽

pp. S144-S148

Author(s):

FABIOLA TERZI ◽

MARTINE BURTIN ◽

GÉRARD FRIEDLANDER

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Transgenic Mice ◽

Renal Injury ◽

Growth Factor Signaling ◽

Renal Lesions ◽

The Past ◽

Epidermal Growth

Abstract. An understanding of the mechanisms underlying the formation of renal lesions is necessary for the development of strategies aiming to delay the progression of chronic renal failure. The generation of transgenic mice in the past 20 years has contributed significantly to the study of this phenomenon. Overexpression and/or inactivation of single factors in renal tissue demonstrated that molecules such as growth factors, proto-oncogenes, and renin-angiotensin system elements play major roles in renal deterioration. Several mouse models of renal injury have been developed in the past 10 yr. Transgenic mice that exhibit a normal phenotype under physiologic conditions allow analysis of the roles of single factors in the progression of chronic renal failure when renal injury models are used. Using this strategy, it was demonstrated that vascular adaptation, which is a process that involves the endothelin/nitric oxide balance, is essential for the survival of mice after nephron reduction and that the epidermal growth factor/activator protein-1/Bcl-2 pathway is involved in the development of renal lesions after renal injury, possibly via adjustment of the proliferation/apoptosis balance. Moreover, it was demonstrated that selective inhibition of epidermal growth factor signaling in the kidney successfully prevents the progression of chronic renal failure. These results indicate the power of transgenesis for elucidation of the pathogenesis of renal disease.

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Effect of Proportional Reduction of Sodium Intake on the Adaptive Increase in Glomerular Filtration Rate/Nephron and Potassium and Phosphate Excretion in Chronic Renal Failure in the Rat

Clinical Science ◽

10.1042/cs0490193 ◽

1975 ◽

Vol 49 (3) ◽

pp. 193-200 ◽

Cited By ~ 2

Author(s):

C. H. Espinel

Keyword(s):

Renal Failure ◽

Glomerular Filtration Rate ◽

Chronic Renal Failure ◽

Glomerular Filtration ◽

Sodium Excretion ◽

Filtration Rate ◽

Sodium Intake ◽

Dietary Sodium ◽

Control Group ◽

Phosphate Excretion

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of ‘autonomous adaptation’ in chronic renal failure is presented.

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Chronic renal failure in a mouse model of human adenine phosphoribosyltransferase deficiency

AJP Renal Physiology ◽

10.1152/ajprenal.1998.275.1.f154 ◽

1998 ◽

Vol 275 (1) ◽

pp. F154-F163 ◽

Cited By ~ 11

Author(s):

Michael G. Stockelman ◽

John N. Lorenz ◽

Frost N. Smith ◽

Gregory P. Boivin ◽

Amrik Sahota ◽

...

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Kidney Disease ◽

Creatinine Clearance ◽

Renal Damage ◽

Male Mice ◽

Adenine Phosphoribosyltransferase ◽

Disease Treatment ◽

Significant Impairment ◽

Normal Males

In humans, adenine phosphoribosyltransferase (APRT, EC 2.4.2.7 ) deficiency can manifest as nephrolithiasis, interstitial nephritis, and chronic renal failure. APRT catalyzes synthesis of AMP from adenine and 5-phosphoribosyl-1-pyrophosphate. In the absence of APRT, 2,8-dihydroxyadenine (DHA) is produced from adenine by xanthine dehydrogenase (XDH) and can precipitate in the renal interstitium, resulting in kidney disease. Treatment with allopurinol controls formation of DHA stones by inhibiting XDH activity. Kidney disease in APRT-deficient mice resembles that seen in humans. By age 12 wk, APRT-deficient male mice are, on average, mildly anemic and smaller than normal males. They have extensive renal interstitial damage (assessed by image analysis) and elevated blood urea nitrogen (BUN), and their creatinine clearance rates, which measure excretion of infused creatinine as an estimate of glomerular filtration rate (GFR), are about half that of wild-type males. APRT-deficient males treated with allopurinol in the drinking water had normal BUN and less extensive visible renal damage, but creatinine clearance remained low. Throughout their lifespans, homozygous null female mice manifested significantly less renal damage than homozygous null males of the same age. APRT-deficient females showed no significant impairment of GFR at age 12 wk. Consequences of APRT deficiency in male mice are more pronounced than in females, possibly due to differences in rates of adenine or DHA synthesis or to sex-determined responses of the kidneys.

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ROLE OF CARDIAC MARKERS IN CHRONIC RENAL FAILURE PATIENTS.

10.36106/ijsr/4303098 ◽

2020 ◽

pp. 81-82

Author(s):

Ramesh Chandra Thanna ◽

B K Agarwal ◽

Rakesh Romday ◽

Neha Sharma

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Positive Association ◽

Morbidity And Mortality ◽

Control Group ◽

High Morbidity ◽

C Reactive Protein ◽

Reactive Protein ◽

Hs Crp

Introduction: Cardiovascular diseases (CVD) are known as important reasons of the increased morbidity and mortality observed in patients with chronic renal failure (CRF). The association of serum Interlukin-6 , homocysteine as well as other cardiovascular risk factors in relation to existence and cause of CVD were investigated. Method: In this study 200 CRF patients were recruited and further stratified into group with Male and Female as case groups. Those without renal failure were assigned as control group (n=200). Results: The patients with CRF showed a significant increase in plasma levels of Cpk-MB homocysteine and C-reactive protein (CRP) compared to control. The positive association were observed between homocysteine, Urea and Hs-CRP, IL_6 . It shows a significant Association of parameters in CRF . Conclusion: The results demonstrated elevation in plasma values IL-6 , homocysteine and HS-CRP in patients with CRF . However, these modifications may be lead to atherosclerosis and consequence CVD event. These parameters may be important with respect to the high morbidity and mortality of CVD found in patients with CRF.

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Familial Atypical Hemolytic Uremic Syndrome with Positive pS1191L (c.3572C> T) Mutation in CFH A Single-Center Experience

10.21203/rs.2.13028/v1 ◽

2019 ◽

Author(s):

Fadime ERSOY DURSUN ◽

Gözde YESIL ◽

Hasan DURSUN ◽

Gülşah SASAK

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Family History ◽

Hemolytic Uremic Syndrome ◽

Atypical Hemolytic Uremic Syndrome ◽

Gene Mutations ◽

Factor H ◽

The Other ◽

History Of ◽

Uremic Syndrome

Abstract Background: Atypical hemolytic uremic syndrome is a condition characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury, which can exhibit a poor prognosis. Gene mutations play a key role in this disease, which may be sporadic or familial. Methods: We studied, 13 people from the same family were investigated retrospectively for gene mutations of familial atypical hemolytic uremic syndrome after a patient presented to our emergency clinic with atypical hemolytic uremic syndrome and reported a family history of chronic renal failure. Results: The pS1191L mutation in the complement factor H gene was heterozygous in 6 people from the family of the patient with atypical hemolytic uremic syndrome. One of these people was our patient with acute renal failure and the other two are followed up by the Nephrology Clinic due to chronic renal failure. The other 3 persons showed no evidence of renal failure. The index case had a history of 6 sibling deaths; two of them died of chronic renal failure. Plasmapheresis and fresh frozen plasma treatment was given to our patient. When patient showed no response to this treatment, eculizumab therapy was started. Conclusions: The study demonstrated that a thorough family history should be taken in patients with atypical hemolytic uremic syndrome. These patients may have familial type of the disease and they should be screened genetically. Eculizumab should be the first choice in the treatment with plasmapheresis. It should be kept in mind that the use of eculizumab as prophylaxis in post-transplant therapy is extremely important for prevention of rejection.

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Effect of chronic renal failure on the hepatic, intestinal, and renal expression of bile acid transporters

AJP Renal Physiology ◽

10.1152/ajprenal.00114.2013 ◽

2014 ◽

Vol 306 (1) ◽

pp. F130-F137 ◽

Cited By ~ 21

Author(s):

Zhibo Gai ◽

Lei Chu ◽

Christian Hiller ◽

Denis Arsenijevic ◽

Carlos A. Penno ◽

...

Keyword(s):

Renal Failure ◽

Bile Acid ◽

Chronic Renal Failure ◽

Plasma Cholesterol ◽

Experimental Studies ◽

Control Group ◽

Early Event ◽

Minor Role ◽

Serum Bile Acid ◽

Protein Levels

Although the kidney is believed to play a minor role in bile acid (BA) excretion, chronic renal failure (CRF) has been reported to be associated with increased serum bile acid levels and alterations in BA homeostasis. The mechanisms for elevated BA levels are poorly understood in both clinical and experimental studies. This study was designed to examine the effects of naturally progressing CRF of longer duration on the hepatic and renal mRNA and protein levels of the BA-synthesizing enzyme Cyp7a1 and the BA transporters Ntcp, Bsep, Mrp3, Ost-α, and Ost-β. Sprague-Dawley rats were randomized to the CRF group (⅚ nephrectomy) or to the sham-operated control group and were analyzed 8 wk after surgery. Results obtained in the CRF rats were compared with those obtained in rats that had undergone uninephrectomy (UNX). The CRF group exhibited significantly increased plasma cholesterol and BA concentrations. Hepatic Cyp7a1 mRNA and protein levels were almost identical in the two groups. Hepatic Mrp3, Ost-α, and Ost-β expression was increased, suggesting increased basolateral efflux of bile acids into the blood. However, no such changes in BA transporter expression were observed in the remnant kidney. In UNX rats, similar changes in plasma BA levels and in the expression of BA transporters were found. We hypothesize that the increase in plasma BA is an early event in the progression of CRF and is caused by increased efflux across the basolateral hepatocyte membrane.

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Uroangiographic Contrast Media-Induced Nephropathy: Correlations between Their Physicochemical Properties and Renal Damage

Urologia Journal ◽

10.1177/039156030507200405 ◽

2005 ◽

Vol 72 (4) ◽

pp. 446-456

Author(s):

C. Alberti ◽

M. Piovano ◽

A. Tizzani

Keyword(s):

Diabetes Mellitus ◽

Renal Failure ◽

Acute Renal Failure ◽

Chronic Renal Failure ◽

Contrast Media ◽

Renal Damage ◽

Contrast Material ◽

Vasoactive Mediators ◽

Adequate Hydration ◽

Hospital Acquired

Contrast media-induced nephropathy (CN) is an important cause of hospital-acquired acute renal failure. Patients with both diabetes mellitus and renal impairment are at high risk. CN pathophysiology involves activation of the tubulo-glomerular feedback and vasoactive mediators such as renin-angiotensin 2, endothelin, adenosine, ADH, etc. The risk of CN can be minimized by the use of non-ionic, low or isoosmolar, contrast material, adequate hydration and prophylactic pharmacological measures. In patients with chronic renal failure who are undergoing arteriography (e.g. coronary angiography and angioplasty), periprocedural hemofiltration appears effective in preventing further renal damage due to contrast agents.

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Endogenous vasopressin regulates Na-K-ATPase and Na+-K+-Cl− cotransporterrbsc-1 in rat outer medulla

AJP Renal Physiology ◽

10.1152/ajprenal.00354.2000 ◽

2002 ◽

Vol 282 (2) ◽

pp. F265-F270 ◽

Cited By ~ 11

Author(s):

Claudia A. Bertuccio ◽

Fernando R. Ibarra ◽

Jorge E. Toledo ◽

Elvira E. Arrizurieta ◽

Rodolfo S. Martin

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Atpase Activity ◽

Receptor Antagonist ◽

The Other ◽

Outer Medulla ◽

Physiological Conditions ◽

Increased Activity ◽

Expression And Activity

Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V2-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 ± 1.5 to 3.7 ± 0.8 in controls ( P < 0.05) and from 19.0 ± 0.8 to 2.9 ± 0.5 μmol Pi · mg protein−1 · h−1 in moderate CRF rats ( P < 0.05). CRF was associated with a significant increase in Na-K-ATPase activity ( P < 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 ± 21.5% compared with controls ( P < 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 ± 9.5 and 105.3 ± 10.9%, respectively ( P < 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 ± 6.5 and 30.0 ± 6.9%, respectively ( P < 0.05), and was not influenced by CRF (95.7 ± 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.

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iTRAQ-Based Proteomics of Chronic Renal Failure Rats after FuShengong Decoction Treatment Reveals Haptoglobin and Alpha-1-Antitrypsin as Potential Biomarkers

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/1480514 ◽

2017 ◽

Vol 2017 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

Yu Yang ◽

Junmeng Wei ◽

Xuekuan Huang ◽

Mingjun Wu ◽

Zhenbing Lv ◽

...

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Differentially Expressed ◽

Coagulation Cascade ◽

Control Group ◽

Differentially Expressed Proteins ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Alpha 1 Antitrypsin ◽

Global Health Problem

Background. Chronic renal failure (CRF) has become a global health problem and bears a huge economic burden. FuShengong Decoction (FSGD) as traditional Chinese medicine has multiple pharmacological effects. Objectives. To understand the underlying molecular mechanism and signaling pathway involved in the FSGD treatment of CRF and screen differentially expressed proteins in rats with CRF treated with FSGD. Methods. Thirty-three male Sprague-Dawley rats were randomly divided into control group, CRF group, and FSGD group. Differentially expressed proteins were screened by iTRAQ coupled with nanoLC-MS/MS, and these identified proteins were later analyzed by GO, KEGG, and STRING. Additionally, haptoglobin (HP) and alpha-1-antitrypsin (AAT) were finally verified by ELISA, Western blot, and real time PCR. Results. A total of 417 proteins were identified. Nineteen differentially expressed proteins were identified in the FSGD group compared with the model group, of which 3 proteins were upregulated and 16 proteins were downregulated. Cluster analysis indicated that inflammatory response was associated with these proteins and complement and coagulation cascade pathways were predominantly involved. The validation methods further confirmed that the levels of HP and AAT were significantly increased. Conclusions. HP and AAT may be the important biomarkers in the pathogenesis of CRF and FSGD therapy.

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Inhibitors of the Fibrinolytic Enzyme System in Renal Disease

Clinical Science ◽

10.1042/cs0390549 ◽

1970 ◽

Vol 39 (5) ◽

pp. 549-557 ◽

Cited By ~ 9

Author(s):

N. B. Bennett ◽

D. Ogston

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Renal Damage ◽

Enzyme System ◽

Normal Subjects ◽

Plasminogen Activation ◽

Significant Elevation ◽

Normal Range ◽

Marked Inhibition ◽

Serum Inhibitor

1. Levels of serum inhibitor of plasminogen activation, anti-plasmin and plasminogen activator were measured in normal subjects and patients with active glomerulonephritis and chronic renal failure. 2. Patients with active glomerulonephritis all had grossly elevated levels of serum inhibitor of plasminogen activation and significant elevation of anti-plasmin. The majority of activator levels lay at the lower end of the normal range. 3. Patients with chronic renal failure had significantly elevated levels of serum inhibitor of plasminogen activation and anti-plasmin, but the changes were less marked than in those with active glomerulonephritis. Activator levels were consistently reduced. 4. The marked inhibition of fibrinolysis in active glomerulonephritis may be a factor in the persistence of glomerular fibrin and ultimately in perpetuation of renal damage. The changes in the fibrinolytic system in chronic renal failure may determine the development of the serosal exudates characteristic of that condition.

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