Genitourinary/Renal System - Summary
Table of all GU conditions organised by history findings, examination findings, investigation findings and management according to Australian guidelines.
Genitourinary; Nikita Goyal
Acute Kidney and Urinary Tract Disease
Acute Tubular Necrosis Acute Tubulointerstitial Nephritis Renal Replacement Therapy Summary
PCT/DCT/Loop of Henle undergo necrosis due to Inflammation of the tubulo-interstitial space by drugs or systemic disease Haemodialysis – more efficient, need to be in
ischaemia or toxins Drugs: Penicillin; Aspirin and NSAIDs hospital, can cause hypotension
Ischaemic: ATN is a Cx of pre-renal AKI Sarcoidosis Peritoneal dialysis - less efficient, can be done at
Toxins: endotoxins (myoglobin – from SLE, HIV home overnight, risk of peritonitis, CI in DM
rhabdomyolysis; bacterial endotoxins) or Systemic inflammatory conditions are more likely to be associated Renal transplant – best option, needs to be
exogenous (gentamicin, NSAIDs) with a nephritis than ATN considered in Stage 4 due to long waiting list +
Muddy brown casts Pyuria, increased RBC’s, increased eosinophils immunotyping, 10yr survival rate is 60%
Info History/RF Examination Investigation Management
AKI Ax – Can be asymptomatic Volume depletion Bedside – Adequate fluid Mx
Sudden loss of Pre-renal (60%) – decreased renal perfusion i.e Oliguria or anuria signs – frank Urinalysis – haematuria, Fluid balance charts
renal function hypovolaemia (dehydration, blood loss), If anuria – renal artery hypotension + proteinuria Fluid restriction – except if
w/ a hypotension (sepsis, CCF, anaphylaxis, thrombosis or post renal tachy, reduced Urine MCS – UTI, casts hypovolaemic shock
consecutive hepatorenal syndrome), renal a stenosis, (FHx of obstruction skin turgor Urine Na, osmolarity – Volume Control – IV fluids (0.9%
rise in Cr and familial hypercholesterolaemia), drugs Pain over bladder or pre-renal AKI (↓Na, saline; colloid – if
blood urea Intra-renal (35%) – acute tubular necrosis, flanks – ‘loin to groin’ Fluid overload ↑osmolarity); intra-renal hypoalbuminaemia)
nitrogen glomerulonephritis, vascular Ax e.g HTN, pain signs – peripheral AKI (↑Na, ↓osmolarity) Diuretics for volume overload –
polyarteritis, cholesterol athero-embolus, acute Incomplete voiding + pulmonary ECG (↑K+) – peaked T frusemide (can exacerbate AKI –
Cr increase tubulointerstitial nephritis Thirst oedema, HTN, HF, waves, increased PR appropriate dosing)
≥26.4µmol/L in Post-renal (5%) – congenital malformations, Fatigue, confusion, SOB interval, wide QRS Consider catheterization – MUST do
48 hrs OR 1.5x BPH, stricture, tumours, nephrolithiasis, blood clot lethargy Bloods – if post-renal Ax
baseline SeCr formation, neurogenic bladder, catheter RF - >65 yrs, CKD, HF, FBE – leukocytosis
associated injuries liver disease, diabetes, Uraemia – (infection), ?
within 7 days anorexia, nausea, Cease nephrotoxic drugs
Pathophys – dementia, prev AKI, thrombocytopenia, ? Stop gentamicin, penicillins,
Pre-renal: ↓ blood supply to kidneys →failure of NSAIDs, gentamicin, encephalopathy, anaemia
Urine output asterixis, cephalosporins, aminoglycosides
renal vascular autoregulation to maintain renal cephalosporins, CRP, ESR Stop ACEi/ARBS
<0.5ml/kg/hr perfusion →↓ GFR → RAAS activation →↑ penicillins, ACEi/ARB, pericarditis UEC – acute Cr rise (up to
for at least 6 (fraction rub), Stop Aspirin/NSAIDs
aldosterone → ↑reabsorption of Na+, H20 →↓ diuretic or hypertensive x3),
hrs urine osmolality ↑ ADH secretion → ↑ etc bleeds (platelet BUN:Cr >100:1 – pre-
AKI Stages reabsorption of H20 + urea Sepsis, iodinated dysfunction) renal AKI; <40:1 – Treat Cx
Intra-hepatic: vascular/tubular nephron damage contrast, excessive fluid intrinsic AKI; ↓ eGFR Hyperkalaemia – ECG monitoring,
→ necrosis or apoptosis of tubular cells →↓ loss – vomiting, Bladder distention ↑K+ (Cx) due to metabolic insulin (push K+ into cells),
reabsorption capacity of electrolytes (Na+), water, diarrhoea, sweating; Pain over bladder acidosis dextrose, calcium gluconate (to
and/or urea → ↑ Na+, H2O in urine →↓ urine haemorrhage, surg, or flanks LFTs stabilise cardiac myocytes),
capacity pancreatitis, trauma, VBG – metabolic acidosis resonium if chronic
Post-renal: bilateral urinary outflow obstruction MPD, nephrolithiasis, amylase/lipase Fluid overload + APO – LMNOP
ASC Consider dialysis – AEIOU –
→↑retrograde hydrostatic p w/ renal tubules → connective tissue Blood culture (is Ax
↓GFR + compression of renal vasculature → disease sepsis) acidosis, electrolytes, intoxication,
acidosis, fluid overload, ↑ BUN, Na+, K+ Clotting? overload, uraemic
GFR will appear normal if one kidney functions Imaging – Anaemic – blood transfusion/EPO
normally US – if obstructive - injections
hydronephrosis
Comps – hyperphosphataemia, hyperkalaemia, CT – retroperitoneal
uraemia, chronic progressive kidney disease, end- pathology of aneurysm
stage kidney disease, acidosis CXR – If CCF suspected
Other –
Urine MCS
UTI Ax - causative organisms – Bacterial – E. coli Dysuria +ive Bedside – Urine dipstick ABX + Analgesia + fluids +
Infections of (approx. 80%), staph saprophyticus (2nd leading ↑ urine frequency costovertebral (nitrites, leukocytes, blood), emptying bladder as much as
the urinary cause of UTI in sexually active women), klebsiella, Urine urgency angle tenderness bladder scan, Urine MCS possible + good hygiene
tract system – proteus, Enterobacter, enterococci, Enterobacter, Haematuria Uncomplicated – Nitrofurantoin (5
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