15. Renal Flashcards
Physiology of the Nephron
- Blood in aorta -> renal artery -> multiple divisions until arterioles -> afferent arteriole forms capillary bed (glomurulus) -> efferent arteriole
- Hydrostatic pressure in glomerulus as efferent arteriole narrower than afferent -> ultrafiltration and formation of urine into Bowman’s capsule -> tubule
- Kidney produces approximately 100mls/min of urine, though majority is resorbed
Anatomy of the Nephron
- Proximal convoluted tubule: Maintain acid-base balance and electrolytes through resorption from filtrate
- Loop of Henle: Concentration of urine (descending limb: sodium and water resorption, ascending limb: impermeable to water, sodium reabsorbed
- Distal convoluted tubule: Fine-tuning of electrolyte balance
- Collecting duct: Water reabsorption due to vasopressin effects
Functions of the kidney (7)
- Removal of waste products/toxins (including drugs, urea & creatinine - muscle breakdown product)
- Balancing of electrolytes
- Stabilizing acid-base status
- Maintaining fluid balance
- Activating vitamin D (1-alpha hydroxylase)
- Stimulating erythropoiesis (erythropoietin produced by juxtaglomerular cells in response to anaemia)
- Maintaining blood pressure (renin)
5/6/7 tend to be affected as a result of chronic kidney disease rather than acute.
Acute kidney injury Definition, what is the Dx based on?
A rapid reduction in kidney function, leading to an inability to maintain fluid, electrolyte and acid-base homeostasis.
Dx based on rise in creatinine +/or decreased urine output
KDIGO diagnostic criteria for AKI:
Rise in creatinine >26μmol/L in 48hrs
Rise in creatinine >1.5 x baseline (best figure in last 3 months)
Urine output <0.5ml/kg/h for >6 consecutive hours
Types of AKI and what they are caused by (broadly)
Pre-renal is most common – hypo perfusion of kidneys. (drugs are NSAID and ACEi/ARBs)
Intrinsic – ATN secondary to pre/post-renal, drugs (Abx, contrast, Caliceurin inhibs, NSAIDs), infiltration (myeloma, amyloidosis).
Post-renal – physical obstruction to urine flow causing increased tubular pressure
Acute kidney injury – pre-renal causes
Often an identifiable cause excessive fluid losses –> decreased renal blood flow (through glomeruli) –> less filtration –> less GFR
General (hypotension/hypovolaemia) Sepsis Major haemorrhage Vomiting/diarrhoea *Congestive heart failure* Renal-specific Renal artery stenosis/embolus Drugs - ACE inhibitors decrease efferent arteriolar constriction, thus decreasing the hydrostatic pressure in glomeruli, reducing filtration. - NSAIDs cause pre-renal AKI by inhibition of prostaglandin production altering glomerular perfusion.
Acute kidney injury – pre-renal signs and symptoms
- Tachycardia
- Hypotension
- Increased capillary refill time
- Clinically dry (decreased skin turgor, absent JVP, dry mucous membranes)
Acute kidney injury – intrinsic renal causes
- Tubular: Acute tubular necrosis (ATN) - 2°to:
- Ischaemia (pre-renal)
- Nephrotoxic drugs (e.g. aminoglycosides)
- Rhabdomyolysis - Glomerular: Glomerulonephritis
- Interstitial: Acute interstitial nephritis (classically NSAIDs)
- Vascular: Vasculitis
Acute kidney injury – intrinsic renal Signs & symptoms:
History of nephrotoxic drug use or long lie/crush injury Rash, petechiae or ecchymoses Nephritic syndrome (oedema, proteinuria & microscopic haematuria)
Acute tubular necrosis
ATN is the commonest intrinsic renal cause of AKI – uncontrolled death of the epithelial cells which line the renal tubules. The dead tubular cells then block the tubule causing increased pressure in the proximal nephron. The high pressure backs up to the bowman’s capsule, and as the pressure gradient between the glomerulus and the tubule is less, less filtration of blood occurs. The dead tubular cells may be seen on urine microscopy as epithelial cell casts. Often secondary to pre-renal damage, myoglobinuria or nephrotoxic drugs.
Acute kidney injury – post-renal causes
Luminal - Stones, Clots, Blocked catheter (LT, old men)
Mural - Benign prostatic hyperplasia, Malignancy of urinary tract, Strictures
Extrinsic compression - Pelvic malignancy, Retroperitoneal fibrosis
Bilateral blockage required - urethral pathology more likely
Acute kidney injury – post-renal Signs & symptoms:
Previous history of urgency, frequency and/or hesitancy
Flank pain +/- haematuria
Distended, palpable bladder if lower urinary tract obstruction
AKI Investigations
- Urinalysis – protein, blood, high specific gravity, cellular casts, culture
- Urea and electrolytes - ↑ creatinine, ↑ urea, ↑ potassium
- Venous blood gas - metabolic acidosis (low pH, low bicarb)
- Renal ultrasound – Unilateral vs bilateral dilated renal calyces (post-renal)
- ECG – signs of hyperkalaemia
Urinalysis results
- Blood + protein suggests glomerular disease
- High specific gravity means urine is concentrated.
- Cellular cast: microscopic cyclindrical structures form in the nephron.
- RBC casts suggests nephritic syndrome (vasculitis/glomerulonephritis).
- WBC casts suggests pyelonephritis or in context of AKI interstitial nephitis.
- Epithelial cell casts an be seen in acute tubular necrosis.
