approach to eq urinary
Approach to suspected renal disease
Presenting signs | · Quiet · Inappetent · Change in urine output | ||
Investigations | · History and clinical exam o On any medications? o Any other clinical signs, e.g. D+ o Exercise intolerance/poor performance? o Any other animals affected? o Any recent surgery? o Can they measure water intake/urine output? o Recent management/dietary changes? · Haematology – TP to assess hydration status, low albumin = PLN · Biochemistry – azotaemia? Ca level usually increased · Urine sample o USG – see if pre/post/renal azotaemia o Urine dipstick – high pH = ARF, high protein = PLN · Abdominal U/S to see kidneys o Enlarged kidneys, painful, perirenal oedema = ARF o Small and hard = CRF o Increased corticomedullary definition = papillary necrosis due to NSAIDs · Renal biopsy if unsure of aetiology, guides prognosis | ||
General management | · IVFT · Diet – balanced protein, low salt, low carb · Increase water intake – add molasses · Stop NSAIDs, oxytet, gentamicin · Re-check USG and renal parameters | ||
ARF vs CKD |
| ARF | CKD |
Presenting signs | · Colic signs · Changes to urine output · Pyrexic · Signs of pre-disposing disease, e.g. D+, SIRS/MODS, myopathies | · Weight loss, reduced appetite · PUPD · Ventral oedema · Dull hair coat | |
Diagnosis | · Increased creatinine · Isosthenuric USG · Proteinuria, haemturia · Enlarged kidneys on U/S · Low calcium, high phosphorus | · Increased creatinine · Isosthenuric USG · Proteinuria · Hypoalbuminaemia · Anaemia · Small kidneys on U/S · Biopsy · High calcium, low phosphorus | |
Treatment | · Stop nephrotoxic drugs · Treat primary cause · IVFT Hartmann’s 2x maintenance | · If glomerulonephritis – steroids and abx · Avoid NSAIDs · Encourage drinking and diuresis – add molasses to water, provide salt lick o IVT not required | |
PUPD | · PD >100ml/kg/day (normal water intake = 50ml/kg/day) · PU >50ml/kg/day (normal urine output = 20ml/kg/day) Causes: · Physiological: lactating mares, working hard, high environmental temperature, excessive dietary protein, excessive salt consumption, drug administration (GCCs, diuretics) · Pathological: apparent psychogenic PD, PPID, CRF, hepatic insufficieny, renal medullary solute washout, sepsis/endotoxemia, DM, DI o APP = most common cause, due to change in diet, stabling, management, environment § Diagnosis: exclusion of other causes (no azotaemia § Treatment: restrict salt and water intake · Iatrogenic: IVFT, diuretics, CS administration, alpha-2s used for sedation, excessive salt in diet | ||
Approach to pigmenturia
History | · Timing of pigmenturia o Beginning of urination = issue with distal urethra o Throughout urination = kidney, ureter or bladder problem o End of urination = issue with bladder or proximal ureter · Any other clinical signs, e.g. signs of infection, myopathies |
Investigation | · Clinical exam · Dipstick urine – is it haem positive or negative o If haem positive ® centrifuge § Clear = haematuria § If discoloured ® look at serum colour · Pink = haemoglobinuria · Normal ® look at CK ® if increased = myoglobinuria o If haem negative ® dipstick for bilirubin § Bilirubin positive = liver disease § Bilirubin negative = drugs · Haematology o TP/PCV – assess hydration state – differentiate between acute/chronic problem o Increased WBC/SAA = infectious/inflammation o Anaemia = EIA · Biochemistry o Evidence of azotaemia – tells us about kidney function · U/S bladder – looking for uroliths · Cystoscopy to directly visualise the bladder |
Management | · Myoglobinuria o IVFT as build up is nephrotoxic o Analgesia o Treat underlying cause · Haemoglobinuria o Treat underlying/primary disease o IVFT if concern for kidneys · Haematuria – treat underlying cause o Urolithiasis – remove o UTI, pyelonephritis – C+S for abx o Idiopathic renal haemorrhage – NSAIDs and TMPS o Urethral rents, neoplasia – surgery |
Causes | · Haematuria o Exercise induced o Urolithiasis o UTI/cystitis o Pyelonephritis o Idiopathic renal haemorrhage o Urethral rents o Neoplasia · Myoglobinuria o Rhabdomyolysis due to muscle injury (myoglobin can leak into plasma) § Exertional rhabdomyolysis § Atypical myopathy § Toxic § Nutritional § Immune-mediated · Haemoglobinuria o Due to ongoing IV haemolysis – due to EIA, immune-mediated, toxins (copper) |