Chronic renal failure (CRF) or chronic kidney disease (CKD) represents the loss of functional renal tissue brought on by an illness that has advanced for more than two months¹. CKD is more frequently observed in geriatric dogs and cats². The loss of nephrons and decreased blood flow to the kidneys with advancing age attribute to an increased risk of renal failure in older dogs. The researchers have reported the highest incidence of renal failure in older dogs (49.58% in >8 years), followed by middle age (35.17% in >4-8 years), and the least in younger dogs (15.25%, <4 years of age)³. The progression of regular wear and tear caused by cellular senescence is held responsible for the gradual development of chronic kidney disease (CKD) among older persons⁴. If CKD is acquired once, it becomes irreparable and causes concerns about reduced renal health⁵. Increased levels of phosphorus, salt, and high-protein diets in both cats and people are also thought to contribute to the development of CKD⁶.

An American bully was presented to the Department of Veterinary Pathology, DGCN COVAS, Palampur, for necropsy examination. A systematic post-mortem examination comprised a detailed external and internal examination of organs. Gross lesions were throughly examined and recorded. The animal passed away while receiving treatment at the DGCN College of Veterinary and Animal Sciences, Palampur. During the necropsy examination representative tissue samples were taken for histopathological examination in 10% neutral buffered formalin (NBF) solution.

After 48 hours of fixation, tissues were processed and stained with haematoxylin and eosin (H&E) stain in accordance with routine histopathological technique⁷.

In the serum biochemical estimation of BUN and creatinine, the values were found to be 95.49 mg/dl and 1.171 mg/dl, respectively. The altered values of BUN and creatinine in serum with reference ranges are presented in Table 1. Gross pathological examination has revealed the presence of subcutaneous oedematous fluid all over the body, or anasarca (Fig. 1), and straw-colouredascitic fluid in the abdominal cavity (Fig. 2). The liver was slightly enlarged and showed diffuse congestion with fibrin. Kidneys showed irregularly elevated blebs on the surface; the renal capsule was tightly adhered to the surface; fluid-filled cavitations were present on the medulla; and the cortex was diminished from the borders due to the disproportionate surface of the kidney (Fig. 3). The spleen was slightly enlarged. The lumen of the intestine exhibited diffuse haemorrhages with catarrhal exudate in the lumen. Histopathological examination of kidneys depicted severe degenerative changes characterised by cellular swelling of tubular epithelium, loss of brush borders, deterioration of tubular epithelium, and the presence of eosinophilic material. Peri-tubular fibrosis and cystic spaces were also documented in the cortical region, along with mononuclear cell (MNC) infiltration (Fig. 4). Liver section was found to show hydropic degeneration, fibrin deposition, engorged sinusoids, and infiltration of MNCs. Intestine showed mild congestion, desquamated mucosa with goblet cell hyperplasia, and infiltration of MNCs.

Some of the studies address the fact that in geriatric dogs, the episodes of renal failure may be worsened by pre-existing diabetes, bacterial pyelonephritis, amyloidiosis, polycystic kidneys, urolith or nephrolith formation, and renal tumours⁸. It has been assumed that, in particular, pathological alterations in relation to hypoxic insults are more frequent in the cortical area of the kidneys as compared with the medulla⁴. In the present study, the elevated levels of BUN and creatinine in serum indicated renal damage⁹. In one of the studies, it was reported that on gross examination, the kidneys were pale, enlarged, and misshapen with an adherent renal capsule¹⁰. The histological picture has depicted marked tubular degeneration, dilated tubules, and the presence of fibrous tissue in the renal parenchyma. These gross and microscopic findings in the kidneys of a dog have a direct correlation with the observations of our study. The fibrous tissue deposition along with degenerative changes in the kidneys of dog in the present study are in concordance with the previous study concluded by the researchers¹¹. It is widely accepted that the reversal of compromised renal function can only be achieved if the tubular basement membrane is intact. Furthermore, more complex hypoxic insults causing damage to the tubular basement membrane support the development of more severe chronic changes⁶. The above-mentioned notions provide widely accepted support for the study conducted by us, as the chronic nephritis recorded in the above case has quite a similar pattern.

In comparison to the general population, patients with CKD have a greater rate of mortality¹². Various epidemiologic studies have certified that even a mild elevation in serum creatinine level is associated with an increased rate of mortality from any cause¹³. Chronic kidney damage may be a substantial risk factor for mortality regardless of comorbid conditions such as diabetes, dietary factors, and hypertension. Further associated conditions and disorders include morbidity and mortality from cardiovascular problems (such as angina, left ventricular hypertrophy [LVH], and increasing heart failure) that are increased by anaemia, which frequently coexists with advancing CKD¹⁴ as represented in Table 2. Disorders of the bones and minerals that are linked to CKD include anomalies in mineral and bone metabolism¹⁵, ¹⁶. Reduced renal phosphate excretion may be attributed to a number of factors. In addition to GFR, the renal tubules additionally serve a role in phosphate reabsorption; damage to the tubules can lead to reduced phosphate excretion. The kidney plays an integral role in phosphate homeostasis by means of the hormone fibroblast growth factor 23 (FGF23), which has the ability to increase phosphate excretion. In Table 2 biochemical test, an increased ALP level was found. In all stages of chronic kidney disease, diabetes is linked to negative outcomes¹⁷.

Chronic kidney damage (CKD) in canines can be of multiple aetiologies, primary ones like dietary imbalance leading to strain on kidneys in the long run, leading to irreversible damage leading to consequences such as renal damage and other deleterious effects like anaemia, as an insult to the kidney will result in diminishing ability to produce erythropoietin, a hormone vital for RBC production; other complications like reduced phosphate will result in hyperphosphatemia and can result in renal osteodystrophy; additionally, cardiovascular risk can be fatal.

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