Introduction

• Cause: in younger animals consider congenital or familial renal disease. In older animals usually acquired, progressive tubulointerstitial nephritis. Results in an inability of the kidney to perform normal functions of waste excretion, fluid/electrolyte/acid-base homeostasis or endocrine function. Some kidney disease may be primarily associated with dysfunction, eg nephrogenic diabetes insipidus, renal tubular acidosis, cystinuria without obvious morphological abnormalities.
• Signs: in early stages (International Renal Interest Society (IRIS) stage I-II) clinical signs may be mild or not detected. With progressive decline in renal function (IRIS stage II-IV) clinical signs can include polyuria/polydipsia and signs associated with uremia (nausea, vomiting, anorexia, oral ulceration, weight loss, constipation). Duration >3 months implies chronicity.
• Treatment: management should be based on IRIS staging (Table 3) but may include phosphate restricted renal diet +/- dietary phosphate binders, gastroprotectants, anti-emetics, anti-proteinuric therapy, subcutaneous/intravenous fluid therapy, erythrocyte stimulating agent, calcitriol, anti-hypertensive therapy.
• Prognosis: early detection of CKD permits management of associated pathophysiological adaptations, eg secondary renal hyperparathyroidism, proteinuria and systemic hypertension, which may slow progression of disease. Management of clinical signs of uremia may improve quality of life.

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Pathogenesis

Etiology

Pathophysiology

• Reduction of functional nephrons → loss of ability to concentrate urine and retention of waste products.
• Hyperfiltration of remaining nephrons → self-perpetuating destruction of remaining nephrons.
• Metabolic acidosis → renal ammoniagenesis → toxic and inflammatory effect on renal interstitium.
• Uremia → erythropoietin deficiency and shortened RBC lifespan → normochromic, normocytic, non-regenerative anemia.
• Hyperphosphatemia Hyperphosphatemia , due to inability to excrete phosphate → hyperparathyroidism → renal osteodystrophy and soft tissue mineralisation (including nephrocalcinosis which may potentiate renal damage).
• Lack of active vitamin D3 (calcitriol) → initiates and exacerbates hyperparathyroidism.
• Proteinuria Proteinuria → increased tubular reabsorption potential to promote tubulointerstitial inflammation → progression of tubulointerstitial nephritis.
• Systemic hypertension → transfer of high systemic pressure to glomerular capillaries → development of glomerular hypertension, glomerular hyperfiltration and glomerulosclerosis → perpetuating renal damage.

Timecourse

• Timecourse is variable and difficult to predict. Some animals can be managed for a long period, while others may show more rapid progression of disease.

Diagnosis

Treatment

Prevention

Outcomes