Acute Renal Failure

Acute renal failure: acute deteriorations of renal function from baseline
- Associated with anuria (almost no urine) and oligouria (passing some urine)
- Sign of uraemia (not symptoms) such as peripheral and lung oedema (accumulation of fluid with no urination), vomiting, nausea, prutitis
- 99% of time, the kidney will recover

• Causes of acute renal failure:
- Pre-renal due to reduction in renal perfusion such as hypovolemia reduced cardiac output, systemic vasodilation and renal vasoconstriction. The kidney is starved of blood and becomes septic and dehydrated.
- Renal: intrinsic damage to tubule, vessels or glomeruli
- Post-renal: due to obstruction downstream by stone or tumour leading to urine retention and reflux. This is damaging to kidney function. Best diagnostic modality is ultrasound

Causes

• Urine microscopy:
- Normal: no protein, rbc, wbc and casts

• Casts: aggregate of particulates within urine and usually formed in distal convoluted tubule or collected duct via precipitation of proteins.
- Conditions of formation: low urine flow, concentrated urine, and acidic environment (damage in tubule)
- Hyaline cast: solidified mucoprotein secreted by tubular epithelial cells
- Granular cast: aggregation of plasma protein such as albumin or cellular cast breakdown
- Red cell casts: presence of red blood cells within cast and indicative of glomerular damage (glomerulonephritis).

Acute tubular necrosis:
- Causes: 90% pre-renal conditions such as sepsis, dehydration, heart failure and low BP. Lack of blood flow compromise viability of cells as renal cells is high ATP dependent.
- Mechanism: urine leaks back into the interstitum and pass to blood.
- Example: car accident causes haemorrhage and decrease in BP. Patients becomes very dehydrated and high creatinine. If resuscitation does not work, the kidney undergoes ATN.
- Drugs: NSAIDs, aminoglycosides and IV contrast all toxic to kidney
- Rhabdomyolysis: muscle injury causes necrosis of cells and release of cytokine which is toxic to kidneys.

• Clinical presentation of ATN:
- Unwell
- oliguric/anuric
- Fluid status variable
- Mid stream urine (no significant red cells or protein, casts present)
- BP variable

• Treatment and progression of ATN:
- Dialysis for up to 6 weeks
- Oliguric phase (damage with GFR loss) to polyuric phase (in recovery phase, GFR restores but tubules can’t absorb fluid)

Rapidly progressive glomerulonephritis: irreversible kidney failure if left untreated (causes are idiopathic)
- Severe immune-mediated injury to kidney’s glomeruli, e.g. anti neutrophils C and anti-GNM antibodies
- Crescentic glomerulonephritis: due to distribution of immune-complex around the basement membrane, glomeruli give a characteristic crescent appearance.
- Crescent formation: capillary rupture from antibody damage leads leakage of plasma protein, with fibrin being the most importance. Fibrin forms clot and epithelial cells of the glomerulus proliferate along with infiltrating leukocytes. Compression of the glomerulus occurs and hence the crescentic scar.

• Clinical presentation of RPGN:
- Unwell
- Acute nephritic syndromes
- Red cell casts and haematuria (antibodies in the kidney damage blood vessels)
- Sign of multi-system disease: haemoptysis (anti-GBM antibodies attach to alveolar, causing damage and pulmonary haemorrhage), rash, arthritis and fever

• Diagnosis of acute renal failure:
- History and examination for pre-renal
- Ultrasound for post renal
- Urine microscopy for sighs of ATN or glomerular disease when others have being excluded
- Biopsy

• Summary:
- Blocked filter is divided into pre-renal, renal, post-renal
- Leaky filter is divided into tubule-interstitial or glomerular
- Both glomerular damage lead to haematuria and proteinuria
- Nephritic syndrome: collection of signs that indicate kidney damage (renal failure)
- Nephrotic syndrome: disorder where the kidney is damaged causing leakage of protein

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