Clinical and hematobiochemical profiling of canine renal failure

Introduction

Renal failure is deterioration of renal function leading to accumulation of nitrogenous wastes due to failure of kidneys to filter waste products adequately from blood (Labato, 2001) [33] . The second leading cause of non-accidental deaths in dogs was renal failure and the average age of onset of renal failure was over 6.9 years in dogs (Lewis et al., 1987) [35] . The presumptive etiology of renal failure in dogs is mainly due to inflammatory causes, pyelonephritis, and ischemic causes and other or unknown (Dunaevich et al., 2020) [15] . The commonest clinical outcomes of acute renal disease in dogs were gastrointestinal abnormalities, which included vomiting, oliguria and anuria, hematuria, halitosis, oral lesions and ulceration (Tufani et al., 2015) [68] . In addition to this the chronic renal failure dogs had other clinical signs viz. polyuria and polydipsia, anemia, loss of body weight, lethargy and depression (Robinson et al., 1989) [49] . Diagnosis of acute renal failure is usually based on the combination of complete history, clinical examination, and laboratory analysis and ultrasound examination. The minimum database for diagnosis of kidney affection includes hematobiochemical examination and imaging techniques. Therefore, this study was planned to evaluate the clinical and haemato-biochemical changes in the renal failure affected dogs.

Materials and Methods

The study was conducted at Department of Veterinary Clinical Complex, Veterinary College, Bidar and Gadag for a period of two years from August 2023 to July 2025. Dogs having signs such as Anorexia, selective or reduced appetite, anuria/oliguria, vomition, polyurea, polydipsia, gradual weight loss, poor hair coat, halitosis, apathy and poor body condition (Ettinger and Feldmen, 2010) [18] Were selected as subjects for the study. A thorough general physical examination was performed clinical parameters such as physical condition, hydration status, colour of the mucous membrane, respiratory rate, heart rate and rectal temperature were documented in the clinical case file. Blood was collected from these dogs and the serum creatinine values were determined and the dogs having serum creatinine>1.4mg/dL were selected for the study group (n=30) and ten apparently healthy dogs with serum creatinine values of ≤ 1.4 mg/dl were selected as control group. Hematological studies were conducted using SMART-3DX Veterinary Hematology Analyzer (Manufactured by Byovet Medical & Technologies Private Limited, India) and biochemistry was carried out with Adiduoplus biochemistry analyzer (Manufactured by ADI Diagnostics Pvt. Ltd, India) through standard procedures described by the biochemical kit manufacturer. Blood urea nitrogen was estimated by Diacetyl monozyme method (Marsh et al., 1957) [38] , and is expressed in units of mg/dL. Serum creatinine was estimated by the modified Jaffe's alkaline picrate method (Folin and Wu, 1919) [21] and concentration of creatinine was expressed as mg/dL. Total plasma protein was estimated by modified biuret and bromo cresol green dye method (Doumas, 1975) [14] and expressed in g/dL. Albumin was estimated by Bromo cresol green end point assay method (Doumas, 1975) [14] and is expressed in g/dL. Potassium is estimated by end point method (Terri, 1958) [66] and is expressed in mEq/L. Microprocessor-controlled electrolyte system that uses ISE (Ion Selective Electrode) technology to make electrolyte measurements was used to measure serum sodium and potassium and the values were expressed as mEq/L. Bicarbonate was estimated as per the procedure described by Tietz (1964) [67] . The values were expressed in mEq/L. This study protocol was reviewed and approved by the Institutional Animal Ethical Committee, (IAEC) of Veterinary College, Bidar. The project proposal number is VCB/IAEC/VMD-16/2023-24. Statistical analysis was performed with GraphPad Prism 8.4 software (GraphPad, CA, USA). The data was presented by using bar diagrams and tables.

Results and Discussion

Clinical Manifestations

In the present study, the most important clinical signs observed in majority of the affected dogs were anorexia (83.33%), lethargy (80%), vomiting (66.67%), dehydration and Oliguria (30.00%), polyuria, and polydipsia (13.33%), pale/anaemic mucosa and gum and weight loss (10.00%), dental tartar and halitosis, malena, hypothermia and oral ulceration (6.67%), haematemesis, ascites, dyspnoea and seizers (3.33%) as enumerated in table 1 and Fig. 1. These findings were in close agreement with those recorded by Cowgill (1995) [7] , Behrend et al. (1996) [2] , Vaden et al. (1997) [71] , Haller (2002) [26] and Kralova et al. (2010) [31] . The uremia typically causes gastrointestinal (GI) signs including nausea, vomiting, diarrhea, anorexia, gastrointestinal and oral ulcerations, with glossitis, stomatitis and halitosis (Nivy et al., 2021) [40] . Oliguria was observed in 30 per cent (n=9) clinical cases of the present study. The development of oliguria involves both hemodynamic and mechanical mechanisms. Hemodynamically, reduced blood volume (hypovolemia) and low blood pressure (hypotension) cause renal vasoconstriction and poor perfusion (Finco et al., 1979; Forrester and Little, 1994) [20,22] . Mechanically, the nephrons may become blocked by thickened cellular casts or compressed by surrounding interstitial edema. These obstructions interfere with the passage of filtrate, ultimately lowering the glomerular filtration rate (Grauer and Lane, 1994; Schulman and Krawiec, 2000) [25,54] . Polyuria and Polydipsia are due to glomerular hyper filtration and systemic hypertension (English, 1973 and Robinson et al., 1989) [17,49] . Anaemia and paleness of mucous membranes were recorded in 10 per cent (n=3) cases and it may be due to decreased production of erythropoietin factor from diseased kidneys, blood loss in the form of hematuria and decreased survival of RBC's due to uremic intoxication (Cowgill, 2003) [5] . Ascites could be due to diminished production of albumin, excretion of proteins through urine or sodium retention by diseases of kidney (Kaneko et al., 2008) [29] . Severe metabolic acidosis leads to tachypnea and increased tidal respiration, decreased cardiac arrhythmias, peripheral arterial vasodilation and central vasoconstriction which can aggravate pulmonary oedma in dogs with renal failure (Shapiro, 1997) [57] .

Physiological parameters

The Mean±SE values of rectal temperature of healthy control group and renal failure dogs were 101.70±0.20 and 101.14±0.22 respectively. This observation suggested that body temperature was not affected but fluctuated within the normal physiological limits in renal failure dogs, which is in agreement with the findings of Elgazzar et al. (2021) [16] . Uremic patients exhibited hypothermia in comparison to nonuremic patients, and the hypothermia also indicated the severity of uremia (Kabatchnick et al., 2016) [28] . In the present study there was significant increase in the heart rate in renal failure dogs (118.50±7.62) compare to healthy dogs (82.80±3.41). But the mean values of heart rate remained in the normal physiological range. Similarly, Sidhu (2015) [59] , Singh (2017) [61] and Dogra (2018) [13] also observed normal mean heart rate in dogs suffering from renal failure. The elevated heart rate in renal failure dogs could be attributed to anemic and dehydration condition of the patients and the values were in the normal physiological range. This was in agreement with the findings of Elgazzar et al. (2021) [16] . The Mean±SE values of respiration rate of renal failure dogs and healthy control dogs were 28.80±1.10 and 26.90±0.87 respectively. This is in agreement with the findings of Elgazzar et al. (2021) [16] and Sidhu (2015) [59] . Respiratory failure alters body buffering mechanism and leads to acute hypercapnia and then chronic hypercapnia causing increased renal excretion of acid. During chronic hypercapnia there is increased resorption of bicarbonate ions by renal tubules in order to maintain increased extracellular bicarbonate ions concentration (Simon and Greco, 1975) [60] .

Hematology

The Mean±SE values of hematobiochemical parameters are enumerated in table 2. The Mean±SE values of hemoglobin, packed cell volume and total erythrocyte count in the healthy control group were 13.85±0.37, 39.85±1.50 and 7.12±0.67 respectively, whereas thhe values were significantly decreased to 10.21±1.02, 30.36±3.45 and 4.19±0.45 respectively in renal failure group of dogs. This was in agreement with Ganesh et al. (1981) [24] , Vaden (2000) [70] , Srivastava et al. (2011) [64] , Devipriya et al.

(2018) [8] , Sumit et al. (2018) [65] and Dunaevich et al. (2020) [15] . Anemia can be seen in ARF due to blood loss in haemorrhage, hemodilution or concurrent infection like leptospirosis that cause anemia and anemia is a feature in CRF due to either reduced erythropoietin secretion (Polzin et al., 1995) [48] or decreased RBC life span, uremic inhibitors of erythropoiesis and external blood loss (Cowgill, 1995 and Osborne et al., 1995) [7,42,44] . The Mean±SE value of Total leucocyte count (TLC) of renal failure dogs was significantly higher (15.86±1.76) compare to healthy control dogs (6.89±0.79). This was in agreement with the recordings of DiBartola et al. (1985) [11] , Benjamin (1986) [3] , Devipriya et al. (2018) [8] and Sumit et al. (2018) [65] . Several researchers have documented leukocytosis in animals suffering from renal failure, including Robison et al. (1989) [73] , Ihle and Kostolich (1991) [27] , Srivastava et al. (2011) [64] , Kavitha et al. (2013) [30] , Devipriya et al. (2018) [8] , and Sumit et al. (2018) [65] . In contrast, Oburai et al. (2015) [41] found no significant differences in total or differential leukocyte counts between dogs with chronic renal failure (CRF) and healthy controls. The elevated TLC in the present study may be due to renal failure caused by leptospirosis, cystitis and inflammatory changes in kidney structures. In renal failure patients, leukocytosis typically reflects inflammatory processes within one or more organ systems. Specifically, when inflammation originates in the urinary tract, it usually involves the parenchymal tissue rather than the excretory pathways (Osborne and Finco, 1995) [19] . Furthermore, underlying systemic conditions that affect the urinary system-such as leptospirosis, bacterial endocarditis, and pyometra are frequently associated with leukocytosis (Osborne et al., 1972; Adin and Cowgill, 2000) [43, 1] . In the present study no significant difference was noticed in platelet count in renal failure dogs (2.56±0.56) and healthy control dogs (3.87±0.54). The mean value of platelets was in accordance with Mann (2013) [37] and Singla et al. (2016) [62] . The observations with respect to platelets in the present study may be due to fewer cases of renal failure having the history of pre-existing Ehrlchiosis (n=6) and Babesisosis (n=3) infection and out of which only four cases were having mild thrombocytopenia.

Biochemistry

The Mean±SE values of biochemical parameters are enumerated in table 2. In the present study, the Mean±SE values of BUN and creatinine in the healthy group were 10.46±1.19 and 0.90±0.09 respectively, whereas they were significantly increased to 54.28±6.09 and 4.06±0.30 respectively in renal failure Group. Similar findings of the study were also observed by DiBartola et al. (1985) [11] , Dighe et al. (1990) [12] , Forterre et al. (2004) [23] and Sumit et al. (2018) [65] . Finco (1995) [19] , DiBartola (2000) [10] and Lefebvre (2011) [34] reported that blood urea nitrogen (BUN) is synthesized in the liver from ammonium and bicarbonate and urea is excreted exclusively by the kidneys. Blood urea concentrations are influenced by factors such as protein catabolism, increased dietary protein intake and urine flow rate. demonstrated that elevated BUN levels are of clinical importance in the detection of renal impairment. Creatinine is produced in muscle through the spontaneous, nonenzymatic breakdown of phosphocreatine and is freely filtered by the glomerulus. Therefore, an increase in plasma creatinine concentration serves as a reliable indicator of impaired renal function and a reduction in glomerular filtration rate (GFR) (DiBartola, 2000 and Haller, 2002) [10,26] , reflecting renal damage. The Mean±SE values of serum phosphorous of all the affected dogs were significantly increased in renal failure dogs (7.14±0.10) compared to healthy dogs (4.63±0.11). Similar findings were also observed by Ross (2011) [51] , Polzin (2011) [46] and Sumit et al. (2018) [65] . Kidneys are the primary route of phosphorus excretion and declining kidney function results in phosphorus retention. Retention of excess phosphorus in the body can promote renal secondary hyperparathyroidism, mineralization of tissues and progression of CKD (Polzin, 2013) [47] . An unaltered change in the values of total protein (TP) in the renal failure dogs (5.98±0. 19) compare to healthy control dogs (6.33±0.32) was observed in the present study whereas, a significant mild hypoalbunemia was noticed in the renal failure dogs (2.50±0.11) compare to healthy control dogs (3.05±0.13). These findings were in close agreement with Seema (2007) [55] and Sumit et al. (2018) [65] . On contrary hypoproteinemia in renal failure dogs was observed by Srikanth and Satish (2014) [63] and Shruti et al. (2017) [58] . Hypoalbuminemia in kidney disease may occur due to urinary protein loss (Polzin, 2010) [45] . In the present study, the Mean±SE values of sodium and potassium in all the healthy control group were 138.60±0.56 and 3.92±0.47 respectively and they were significantly increased to 148.79±1.26 and 4.73±0.13 respectively in renal failure group. Although a statistically significant difference was observed in the mean sodium and potassium concentrations in between the two groups the mean sodium and potassium values in the present study remained within normal physiological limits in the affected dogs. These findings are consistent with the report of Schaer (1995) [53] , who stated that serum sodium concentrations generally remain normal in patients with uremia. Neither hypernatremia nor hyponatremia was recorded during the present investigation. Nevertheless, disturbances in sodium balance may occur when there is an imbalance between body water and sodium, particularly in oliguric patients or following inappropriate fluid therapy. Similar observations have been reported by Rubin (1995) [52] , Schaer (1995) [53] , Cowgill and Francey (2005) [6] and Seema (2007) [55] . The Mean±SE values of bicarbonate in the renal failure and healthy dogs were 17.20±0.45 and 20.82±0.39 respectively, where a significant decrease in the bicarbonate values was recorded in renal failure group. These findings were in agreement with Chambers (1987) [4] , Ross (1989) [50] , McGrotty (2008) [39] , Vijay et al. (2011) [72] , Lippi et al. (2023) [36] and Segev et al. (2024) [56] . The metabolic acidosis in AKI results from increased acid generation, decreased bicarbonate reabsorption, and decreased acid secretion. High anion gap metabolic acidosis is also recognized with hyperlactatemia (associated with decreased tissue perfusion) in human and veterinary patients secondary to both diabetic ketoacidosis and toxin ingestion (e.g. ethylene glycol) (Ueda et al., 2015) [69] . Metabolic acidosis can also be caused by loss of HCO3-rich fluid from the body, addition of fixed acid to the body or its production by metabolism within the body or failure of renal excretion of fixed acid from the body. Loss of HCO3-rich fluid usually occurs via the gastrointestinal tract (e.g., small bowel diarrhea), but it also may occur via the kidneys (e.g., carbonic anhydrase inhibitors, proximal renal tubular acidosis) (DiBartola, 2012) [9] .

Conclusion

Renal failure in dogs is characterized by prominent clinical signs such as anorexia, vomiting, lethargy and altered urination patterns, along with significant hematobiochemical alterations. The study revealed anemia, leukocytosis, azotemia, hyperphosphatemia, mild hypoalbuminemia and decreased bicarbonate levels indicating metabolic acidosis. Physiological parameters largely remained within normal limits despite statistical variations. These findings emphasize that a combination of clinical evaluation and hematobiochemical profiling is essential for accurate diagnosis, assessment of disease severity and effective management of renal failure in dogs.

Acknowledgement

AcknowledgmentThe authors are very much thankful to the support extended by the Institute for providing necessary facilities to carry out this study.

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