Renal and urology Flashcards
Acute kidney injury (AKI)
Rapid drop in kidney function, criteria:
- ↑ creatinine > 25 micromol/L in 48 hours
- ↑ creatinine > 50% in 7 days
- Urine output < 0.5 ml/kg/hour over at least 6 hours
Risk factors for AKI
- Older age (e.g., above 65 years)
- Sepsis
- Chronic kidney disease
- Heart failure
- Diabetes
- Liver disease
- Cognitive impairment (leading to reduced fluid intake)
- Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
- Radiocontrast agents (e.g., used during CT scans)
Causes of AKI
Pre-renal (insufficient blood supply), renal (kidney disease) and post-renal (outflow obstruction)
Pre-renal: dehydration, shock, HF
Renal: glomerulonephritis, haemolytic uraemic syndromw, rhbdomyolysis
Post-renal: kidney stones, tumours, BPH, neurogenic bladder
Investigations for AKI
Urinalysis
- Leucocytes + nitrites = infection
- Protein + blood =acute nephritis (but can be positive in infection)
- Glucose = diabetes
Ultrasound of the urinary tract to look for obstruction if post-renal cause suspected.
Management for AKI
- Avoid/stop nephrotoxic drugs1
- Adequate fluids (IV or oral)
- IV fluids for dehydration/hypovlaemia
- Withhold/adjust meds that may accumulate in AKI (e.g. opiates, metformin)
- Relieve obstruction if post-renal e.g. catheter in BPH
- Dialysis and renal input if severe
DAMN: diuretics, ACEi/ARB/metformin, NSAIDs
ACEi not strictly nephrotoxic, stop in AKI as they reduce filtration pressure, but ACEi are renal-protective in the long-term
Complications of AKI
- Fluid overload, heart failure and pulmonary oedema
- Hyperkalaemia
- Metabolic acidosis
- Uraemia (high urea) > encephalopathy and pericarditis
Diabetes insipidus
Antidiuretic hormone (ADH) or arginine vasopressin (AVP) produced in hypothalamus and secreted by posterior pituitary gland. ADH stimulates water reabsoprtion from kidney collecting ducts.
DI caused by:
- A lack of ADH (cranial DI)
- A lack of response to ADH (nephrogenic DI)
Kidneys cannot reabsorb water and concentrate urine = polyuria (>3L/day), polydipsia, dehydration and postural hypotension
Causes of nephrogenic DI
When collecting ducts of kidneys do not repsonse to ADH:
- Idiopathic
- Medications particularly lithium
- Genetic mutations in ADH receptor gene (X-linked recessive)
- Hypercalaemia
- Hypokalaemia
- Kidney disease (e.g. PKD)
Causes of cranial DI
When hypothalamus does not produce ADH for the pituitary gland to secrete
- Idiopathic
- Brain tumours
- Brain injury
- Brain surgery
- Brain infections (e.g. meningitis)
- Genetic mutation in ADH gene (autosomal dominant)
Investigations for Dibates Insipidus
Water deprivation test (desmopressin stimulation test) is diagnostic test
Patient avoids fluids for 8hrs, then patient given synthetic ADH (desmopressin) depending on result, see graph
Management of DI
- Treat underlying cause e.g. stop lithium
- Cranial DI = desmopressin
- ## Nephrogenic DI: plenty of fluids, high-dose desmopressin, thiazide duretics, NSAIDs
Chronic kidney disease
Chronic reduction in kidney function sustained over three months, permanant and progressive
Causes that speed up decline:
- Diabetes
- HTN
- Medications (NSAIDs or lithium
- Glomerulonephritis
- PKD
Presentation of CKD
Asymptomatic until later
- Fatigue
- Pallor (anaemia)
- Foamy urine
- Nausea
- Loss of apetite
- Pruritus
- Oedema
- HTN
- Peripheral neuropathy
Classification of CKD
Diagnosis made when results are sustained over at least three months:
- Estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2
- Urine albumin:creatinine ratio (ACR) > 3 mg/mmol
Management of CKD
- Kidney Failure Risk Equation used to estimate 5-year risk of kidney failure needing dialysis.
- Treat excebating conditions
- Aim BP <130/80 if under 80
- ACEi/ARB/dapagliflozin to slow disease progression
- Exercise, maintain healthy weight and avoid smoking
- Atorvastatin 20mg for CVD prevention
- End-stage: special diet, dialysis, renal transplant
Complications of CKD and their treatments
- Anaemia (lack of erythropoietin) - recombinant human erthropoietin
- Renal bone disease: high phosphate, low vit D activity, low serum calcium
Mx: low phosphate diet, phosphate binders, active forms of vit D (e.g. calcitriol)
Adequate calcium intake
1 CKD =
- Reduced phosphate excretion = high Ph
- Reduced vit D metabolism, essential for calcium absorption in intestines and reabsorption in kidnets
Epididymo-orchitis
Inflammation of the epididymis and testicles due to infection
- E-coli
- Chlamydia trachomatis
- Neisseria Gonorrhea
- Mumps - think mumps if patient has parotid gland swelling and orchitis (spares epididymis
Presentation of epididymo-orchitis
Gradual onset - mins - hours
- Testicular pain
- Dragging sensation
- Swelling
- Tenderness on palpation - paritcularly epididymia
- Urethral discharge (suspect chlamydia/gonorrhoea)
- Systemic symptoms e.g. fever/sepsis
Diagnosis of epididymo-orchitis
Enteric (E.coli) or STI (chlamydia/gonorrhoea)
RFs for STI: < 35, ↑ sexual partners, urethral discharge
Ix:
- Urine microscopy, culture and sensitvitiy (MC+S)
- Chlamydia and gonorrhoea NAAT testing, - Charcoal swab of discharge for gonorrhoea C+S
- Serum antibodies + saliva swabs if mumps
- USS for torsion or tumours as ddx
Mx of epipdymo-orchitis
- Septic/very unwell = hospital for IV abx
- Urgent referral to GUM for assessment and tx
- Abx according to local guidelines
- Eenteric (E.coli) - ofloxacin/levofloxacin/co-amoxiclav if CI
- Empirical tx for STI usually combination of IM ceftriaxone single dose, doxycycline, ofloxacin
Quinolones are powerful broad-spectrum abx
Main SEs: tendon damage and rupture, particular achilles. Lower seizure threshold, CI in epilepsy
