Pathology Cheat Sheet
Follow the Nephron Loss
Renal failure for NEET-PG: prerenal vs intrinsic vs postrenal, acute tubular necrosis phases, muddy brown casts, and chronic kidney disease consequences.
MedNext Academy | 3 min read
Follow the Nephron Loss
Renal failure for NEET-PG: prerenal vs intrinsic vs postrenal, acute tubular necrosis phases, muddy brown casts, and chronic kidney disease consequences.
Acute kidney injury including acute tubular necrosis, and the pathology and consequences of chronic renal failure.
High-yield lines
- Acute kidney injury is classified as prerenal, intrinsic renal, or postrenal.
- Prerenal azotaemia arises from hypoperfusion with a raised urea-to-creatinine ratio and low urinary sodium.
- Acute tubular necrosis is the most common intrinsic cause of acute kidney injury.
- Ischaemic acute tubular necrosis affects the straight proximal tubule and thick ascending limb.
- Nephrotoxic acute tubular necrosis is caused by aminoglycosides, radiocontrast, and heavy metals.
- Muddy brown granular casts in the urine are characteristic of acute tubular necrosis.
- Acute tubular necrosis passes through initiation, maintenance oliguric, and recovery polyuric phases.
- Because tubular basement membranes are preserved, acute tubular necrosis can recover with epithelial regeneration.
- Chronic renal failure produces small contracted granular kidneys with glomerulosclerosis and tubular atrophy.
- Chronic kidney disease causes normocytic anaemia from reduced erythropoietin and renal osteodystrophy.
- Uraemia causes pericarditis, encephalopathy, and platelet dysfunction with bleeding.
- Diabetes and hypertension are the leading causes of chronic kidney disease.
Mapped competency codes
- PA28.3
- PA28.4
- PA28.9
Continue into the full chapter
This summary maps to PA28-urinary-tract.
Frequently Asked Questions
What is the most common intrinsic cause of acute kidney injury?
Acute tubular necrosis, resulting from ischaemia or nephrotoxins, and characterised by muddy brown granular casts in the urine.
Why can acute tubular necrosis recover?
Because the tubular basement membrane is preserved, allowing surviving epithelial cells to migrate and regenerate along the intact scaffold during the recovery phase.
What distinguishes prerenal azotaemia?
A raised urea-to-creatinine ratio and low urinary sodium, reflecting renal hypoperfusion with intact tubular concentrating function.
What systemic effects does chronic kidney disease produce?
Normocytic anaemia from erythropoietin loss, renal osteodystrophy, and uraemic complications such as pericarditis and platelet dysfunction.
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