UDDT Dysfunction

Pathogenesis of CKD

Kidneys become damaged, loss of nephrons (functional part), not many CS at first, as it progresses - more nephron loss leads to onset of CS

Idiopathic CKD

Less effective filtration leads to increased renal blood flow and increased urine production due to increased thirst to keep fluid balance. Fewer toxins can be removed by kidneys

Causes of non-idiopathic CKD

Infection (pyelonephritis)

Urolithiasis (obstruction)

Neoplasia (renal lymphoma/carcinoma)

Delayed AKI tx

CKD Clinical Signs

PU/PD - first sign! Compensating for renal failure, inability to concentrate urine = PU

Lethargy - strain on organs & dehydration, weight loss / decreased appetite

Anaemia - decreased erythropoietin production

Anorexia - toxins = nausea

Halitosis & oral ulcers

Hypertension - decreased renal BF = RAAS (Renin-Angiotensin-Aldosterone System), vasoconstriction

Hypokalaemia

Low head carriage

Sunken eyes, tacky MM, skin tenting

CKD Tx / Nursing

Long term management, aim to decrease azotaemia and proteinuria to delay progression.

IVFT - correct dehydration, flush toxins, maintain renal perfusion

Increase per os fluid —- wet food

Diet - decrease / restrict protein to decrease renal workload, high quality protein source!!

ACE inhibitors - use with caution

Ureterolithiasis

SUB placement / management

Diagnosing Renal Disease

GFR - correlates directly with renal function, complex test

Azotaemia - increased nitrogenous waste in blood (creatinine, urea, phosphate)

Proteinuria - increased = renal damage, less effective filtering of proteins in blood

AKI Pathophysiology

Acute kidney injury - rapid and severe loss, body can’t respond, very sick very quick

Tx possible

AKI can develop on top of CKD

Uni or bilateral

Pre-renal AKI

Insult before kidney

Decreased blood to kidney

Can be reversible

Causes: hypotension, anaesthesia, NSAID use, ACEi, circulatory shock

Renal (intrinsic) AKI

At kidney

Most difficult to treat - immediate tx, 18hr+ often irreversible

Causes: toxins!! - lilies / antifreeze (cats), raisins (dogs)

Secondary to: infection, cancer, dental do, pancreatitis, FIP, diabetes

Post Renal AKI

Lower in urinary tract

After BF to kidney

Causes: obstruction (stops micturition), increased toxins = renal damage

AKI Clinical Signs

More varied, cause dependent

PU/PD

Depression

Lethargy

Anorexia

V+

Halitosis

Anura/oliguria

Hyperkalaemia due to oliguria

Stranguria

Bradycardia - caused by increased K+

Neurological signs

AKI Tx

Age appropriate nutrition

Careful of nephrotic drug use

Optimum BW

High IVFT rate - correct acid base imbalance

Monitor UOP. —- INS & OUTS

Correct oliguria - catheter

Toxins - emesis / charcoal

Infection - antibiotics / culture

Prevention better!!