Bilateral juvenile renal dysplasia in a Norwegian Forest Cat

2009 ◽  
Vol 11 (4) ◽  
pp. 326-329 ◽  
Author(s):  
Luca Aresu ◽  
Renato Zanatta ◽  
Paola Pregel ◽  
Diego Caliari ◽  
Massimiliano Tursi ◽  
...  

Renal dysplasia is defined as a condition of disorganised development of renal parenchyma due to abnormal differentiation. The case of a 5-month-old intact male Norwegian Forest Cat with a history of polyuria and polydipsia is reported. Ultrasonographic examination showed a slight enlargement of kidneys. Biochemical parameters, haematological examinations and clinical signs were compatible with chronic renal failure (CRF). Histological examination was correlated with a primary tubular disorganisation and modification of glomerular compartment. The clinical history together with the histological lesions is consistent with bilateral juvenile renal dysplasia in this cat. To our knowledge, feline renal dysplasia has been reported in fetal infections with panleukopenia virus; no reports indicate the idiopathic origin in feline dysplastic lesions.

2017 ◽  
Vol 45 ◽  
pp. 5
Author(s):  
Samara Rosolem Lima ◽  
Leilane Aparecida Da Silva ◽  
Geovanny Bruno Gonçalves Dias ◽  
Letícya Lerner Lopes ◽  
Raquel Aparecida Sales Da Cruz ◽  
...  

Background: Renal dysplasia, which has been reported in some dogs and human patients, refers to a developmental disorder of renal parenchyma due to imperfect inductive interaction between the mesonephric duct and the metanephric blastemal. In dogs, the characteristic histological findings on which diagnosis is based include (1) persistent metanephric ducts surrounded by primitive mesenchyme, (2) fetal or immature glomeruli, (3) fetal or immature tubules, and (4) anomalous presence of interstitial fibrous tissue. The aim of this study was to report the major pathological and immunohistochemical features of nine young dogs necropsied with renal dysplasia.Cases: The necropsy files from the Laboratório de Patologia Veterinária (LPV) of the Universidade Federal do Mato Grosso (UFMT) were reviewed between the years 2008 and 2013. Dogs diagnosed with chronic kidney failure and macroscopic and histopathological renal lesions consistent with renal dysplasia were selected. Kidney fragments in paraffin blocks were cut and stained with hematoxylin and eosin and by immunohistochemistry (IHC) using anti-vimentin and anti-cytokeratin monoclonal antibodies. The staining was considered positive for the presence of at least one renal cell marked with brown cytoplasmic staining clear and unambiguous. A total of 787 necropsies of dogs were performed. Of these, 64 had a clinical diagnosis of chronic renal failure of which 9 were classified as renal dysplasia. The age of the dogs ranged from 3 months to 2 years. Clinical signs were characterized by anorexia and non-regenerative anemia in 88.9%, vomiting 66.7%, dehydration 55.6%, uremia 55.6%, convulsion 33.4%, abdominal pain 22.3% and diarrhea in 11.2% of cases. At necropsy the main macroscopic changes in the kidneys were external surface with pale staining, in 6 of 9 dogs necropsied. Additionally, 5 dogs, cystic cavities of various sizes from 0.1 to 5 cm in diameter, diffusely distributed in the renal subcapsular surface and cutting were observed. Of the 64 dogs with diagnosis of chronic renal failure, 14.06% had dysplastic kidney changes, characterized by dilatation of Bowman’s space, glomerular and tubular atrophy, immature glomeruli and tubules, lymphocytic interstitial inflammation and fibrosis. In the dogs with renal dysplasia, it was observed that the tubular structures showed marked glomerular labeling for vimentin. Moreover, the kidneys of normal dogs showed weak or absent for marking tubes and glomerular structures for vimentin, and strong staining for cytokeratin in tubular cells, glomerular cells and collecting ducts.Discussion: Renal morphological damage observed in these nine dogs less than two years old, that contained degenerative and inflammatory changes, fibrosis and glomerular atrophy, but mostly immature glomeruli and tubules were associated with atypical renal dysplasia. This condition develops when the urethral diverticulum and metanephric blastoma not properly form in the embryonic stage, resulting in abnormal metanephric differentiation and formation of structures that do not recapitulate the normal nephrogenesis. Abnormal kidney function in young animals caused chronic renal failure resulting in death. The results of immunohistochemical observed in this study can complement the diagnosis of renal dysplasia. The morphological normality can be observed in the proportion of mesenchymal and epithelial tissue in the different structures of the kidney by staining with anti-cytokeratin and anti-vimentin. In the present study, there was moderate to strong labeling of vimentin in glomerular and tubular structures being dysplastic kidney would be expected to occur in normal dogs predominant staining with cytokeratin. Based on the clinic, pathological and immunohistochemical findings it is concluded that the animals developed renal dysplasia.


2019 ◽  
Author(s):  
Fadime ERSOY DURSUN ◽  
Gözde YESIL ◽  
Hasan DURSUN ◽  
Gülşah SASAK

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.


2000 ◽  
Vol 2 (2) ◽  
pp. 75-82 ◽  
Author(s):  
D J Polzin ◽  
C A Osborne ◽  
S Ross ◽  
F Jacob

Dietary modification is of primary importance in managing cats with chronic renal failure. Diets designed for cats with chronic renal failure are typically formulated to be pH neutral and contain reduced quantities of protein, phosphorus and sodium and an increased quantity of potassium. These changes in diet formulation are designed to ameliorate clinical signs of renal failure by adapting dietary intakes to meet the limited ability of failing kidneys to adapt to the normal range of dietary intakes. Important recent clinical trials support the therapeutic value of dietary therapy in cats with chronic renal failure.


1988 ◽  
Vol 11 (3) ◽  
pp. 238-247 ◽  
Author(s):  
Raymond M. Hakim ◽  
J. Michael Lazarus

2009 ◽  
Vol 54 (No. 5) ◽  
pp. 236-243 ◽  
Author(s):  
S. Kralova ◽  
L. Leva ◽  
M. Toman

Chronic renal failure causes immunosuppression in people and is thought to be one of the causes of non-infectious secondary immunosuppression in dogs. The purpose of this study was to evaluate changes in counts and activity of polymorphonuclears in dogs with chronic renal failure in various stages. Haematological, biochemical examinations and examination of non-specific immune response cells (total and differential leukocyte counts, phagocytosis of methacrylate particles, chemiluminescence test, and level of lysozyme) were performed in blood samples obtained from these dogs. Neutrophilia, lymphopoenia and a decreased number of eosinophils in comparison with healthy control were the main findings in groups with clinical signs. We found the statistically highly significant elevation of lysozyme level; it was in a strong positive correlation with the level of urea, creatinine and phosphorus. We did not find any statistically significant changes in phagocytosis process and other serological factors. In conclusion, despite the reports from human medicine, chronic renal failure in dogs does not alter phagocytosis. From this aspect, the elevation of lysozyme level is the main effect of uraemia.


2008 ◽  
Vol 53 (No. 12) ◽  
pp. 660-667 ◽  
Author(s):  
E. Ludvikova ◽  
I.D. Wijnberg ◽  
P. Fictum ◽  
Z. Lukas ◽  
J.H. van der Kolk ◽  
...  

Objective of the study was to assess histopathological changes in horses with a clinical history of exertional rhabdomyolysis (ER) with special reference to polysaccharide storage myopathy and to compare histopathological findings in horses with and without a clinical history of ER. In total 39 muscle samples were collected, from horses with a history of repeated episodes of exertional rhabdomyolysis (test group, 10 horses) and from horses without clinical signs of muscular disorders in their history (control group, 29 horses). Frozen muscle samples were stained with haematoxylin and eosin and periodic acid-Schiff with and without amylase digestion. Histopathologic changes (amylase resistant polysaccharide, subsarcolemmal glycogen, intracytoplasmic masses, subsarcolemmal vacuoles, fibre size variation and internal nuclei) were evaluated. There was a statistically significant difference between groups in the presence of subsarcolemmal amylase sensitive glycogen deposits (P ≤ 0.0001), the risk ratio was 5.22. Statistically significant differences between groups were not found regarding the presence of intracytoplasmic masses, subsarcolemmal vacuoles, amylase resistant polysaccharide, fibre size variation and internal nuclei. Presence of amylase resistant polysaccharide within muscle fibres of apparently healthy horses could be a manifestation of different phenotype expression of PSSM but also the insufficient specificity of this diagnostic criterion.


2012 ◽  
Vol 43 (1) ◽  
pp. 153-158 ◽  
Author(s):  
Gwen Jankowski ◽  
Jennifer N. Langan ◽  
Michael J. Adkesson ◽  
Karen A. Terio ◽  
Natalie D. Mylniczenko ◽  
...  

1978 ◽  
Vol 54 (2) ◽  
pp. 133-140 ◽  
Author(s):  
S. Scherrer ◽  
B. Haldimann ◽  
A. Küpfer ◽  
F. Reubi ◽  
J. Bircher

1. To evaluate potential alterations in hepatic metabolism of drugs occurring in patients with renal insufficiency the fate of aminopyrine was studied in 17 patients with chronic renal failure and in 27 normal subjects. 2. Although patients with chronic renal failure exhibited large variations, their aminopyrine plasma disappearance times (mean 0·62 ± sd 0·24 h−1) were significantly higher than those found in normal subjects (0·30 ± 0·07 h−1, P < 0·002). 3. 14CO2 derived from [dimethylamine-14C]aminopyrine disappeared from breath more rapidly in patients with chronic renal failure and a history of analgesic abuse (0·40 ± 0·04 h−1) than in control subjects (0·22 ± 0·03 h−1, P < 0·01) and in other patients with chronic renal failure (0·24 ± 0·04 h−1). 4. Dialysis treatment and serum creatinine concentrations were not correlated with the rates of aminopyrine metabolism. Two additional patients, however, with combined renal and hepatic disease, exhibited markedly slowed rates of aminopyrine demethylation. 5. Although chronic renal failure by itself might not alter microsomal drug metabolism it is concluded that, in patients with a history of abuse of phenacetin-containing analgesics, marked acceleration in aminopyrine N-demethylation may be observed.


2021 ◽  
Vol 53 (03) ◽  
pp. 259-264
Author(s):  
Mohammed Abed Jawad ◽  

Background: The current research is designed to investigate alterations in lipid peroxidation (malondialdehyde - MDA) and renal markers (urea and creatinine) in patients of chronic renal failure (CRF) as compared to the control group. Method: The study included 55 subjects, who were separated into two groups: control group, which included 15 healthy members with no history of systematic illness; and patients group, which included 40 patients with CRF divided into four groups “Non: CRF patients without any accompanied disease, DM: CRF patients with diabetes mellitus, HT: CRF patients with hypertension, and HT + DM: CRF patients with diabetes mellitus and hypertension”. Results: The findings reveal that there is a notable increase in serum concentration of MDA, urea, and creatinine, in patients group as compared to the control group. Conclusion: In all chronic renal failure patients with or without any accompanying disease, lipid peroxidation is present in pre- and post-haemodialysis patients as well as patients with CRF have high levels of urea and creatinine compared with healthy groups.


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