Sorry I don't have a good source for you - but here is how I see it approached most often on the wards. I hope you find it helpful -
I. Decide if acute vs. chronic (using baseline/serial creatinine is simplest)
---A) Acute renal failure: Decide if prerenal, intrinsic renal or postrenal. Most important calculation here is fractional excretion of sodium (FeNa), most important test is the "Liquid Biopsy," i.e. the UA. Renal US may be useful.
-----1) Prerenal: the kidney is not sufficiently perfused (e.g., shock, congestive heart failure). In this case the kidney will be sodium avid and fractional excretion of sodium (FeNa = (UNa * PCr)/(UCr * PNa)), all x 100) will be low, < 1%. UA will show a high specific gravity and is "bland" - hyaline casts may be seen.
-----2) Intrinsic renal: there are a million causes for this; try to decide if pt is in ATN, nephrotic, or nephritic. Use UA and FeNa.
--------a) ATN (acute tubular necrosis): most common cause of ARF in the hospital. Prolonged hypotension causes the tubules to slough; it can also be caused by contrast and assorted other toxins (nephrotoxic abx/chemo drugs, rhabdomyolysis, etc.). FeNa is high (>3%). UA shows mild proteinuria and microhematuria (since the normal blood/urine barriers have been disrupted) granular, "muddy brown" casts and renal epithelial cells can also often be seen.
--------b) Nephrotic syndrome: Losing more than 3g/day of protein in the urine. Rather than the 24 hour urine collection, spot urine protein:creatinine ratio gives a good estimate of 24 hour urine protein excretion. Pt also has decreased serum albumin, hyperlipidemia, lipiduria, edema. Common causes include (there is a long list) minimal change disease, focal segmental glomerulosclerosis (think about this in an HIV+ pt w/azotemia, nephrosis).
--------c) Nephritic syndrome: represents inflammation of the glomeruli. UA will show an "active sediment" with blood (often gross blood with white cells and dysmorphic RBC's), protein, and red cell casts. Patients will usually be edematous and hypertensive. Another long list of possible causes including Goodpasture's, Wegener's, lupus, HUS...many of the etiologies are autoimmune or post-infectious, I am not going to get into all the immunologic testing - p-ANCA, complement levels, etc. Renal biopsy is often helpful in these patients.
-----3) Postrenal: urinary tract is obstructed below the kidneys. Always think of this in an anuric or oliguric patient. Renal ultrasound will show hydronephrosis; pts will often enter a diuretic phase after the obstruction has been relieved. The classic situation is an old man w/BPH, and a history of slow urinary stream/anuria. Foley catheterization yields copious urine. In a pt with 2 functional kidneys the obstruction is most likely in the bladder or urethra, however there are situations (e.g., large pelvic/abdominal mass) where both ureters can be infiltrated/compressed.
---B) Chronic renal insufficiency. Look for conditions in the patient's medical history that would predispose them to renal failure, including diabetes, hypertension, HIV, heroin use, systemic inflammatory disease (lupus), heay NSAID use, family history. I think a basic workup would include renal ultrasound (big cystic kidneys vs. tiny, shrunken kidneys); HbA1c; urine microalbumin; CBC (CRF pts are usually anemic); CMP (hyperphosphatemia/hypocalcemia); UA (may see broad casts; often bland); renal artery imaging (US or MRA, highest yield probably in pts w/intractable hypertension). If the patient is anemic, SPEP and UPEP should be obtained to look for paraproteinemia (multiple myeloma). Renal biopsy when the cause cannot be elucidated.
