HY lecture notes:
Sulfa drug or gold salts + kidney issue + no blood in urine; Dx? –> membranous glomerulonephropathy (MG).
Biopsy finding in MG? –> subepithelial deposits; “spike and dome” appearance is prevalent in resources / Qbank but buzzy and not on the NBMEs.
HepB or C + nephrotic syndrome; Dx? –> MG –> usually due to HepB.
Autoantibodies in membranous glomerulonephropathy? –> sometimes patients are positive for anti-phospholipase A2 receptor antibodies.
HepC + nephritic syndrome; Dx? –> MPGN.
Multiple myeloma + renal diagnosis? –> renal amyloidosis –> immunoglobulin light chains in high levels moving through the kidney (Bence Jones proteinuria) leads to deposition in the renal parenchyma. You should memorize the sentence: “Multiple myeloma is the most common cause of renal amyloidosis.”
First change in the kidney with diabetes? –> hyperfiltration –> increased filtered glucose pulls water with it.
First histologic change in the kidney with diabetes? –> thickening of the glomerular basement membrane –> due to non-enzymatic glycosylation of basement membrane. If the question asks you for the first renal change seen overall in diabetes, select hyperfiltration.
USMLE Q mentions guy with diabetes + polyuria; asks why he has increased urinary output –> answer = “increased glomerular filtration rate.”
Amount of glucose reabsorbed in PCT? –> 100% physiologically; glycosuria not seen until serum levels exceed around 180 mg/dL.
Late finding seen histologically in diabetic nephropathy? –> Kimmelstiel-Wilson nodules.
What are KW nodules composed of? –> hyaline à HY on Step 1 for some reason; don’t confuse this fibrin, which is the answer for the crescents in RPGN.
Example of type II diabetes drug that acts in the kidney? –> Dapagliflozin (SGLT2 inhibitor in PCT; prevents reabsorption of glucose).
What is hyaline arteriolosclerosis? –> hyaline deposition in the arterioles of the kidney usually seen in diabetes –> non-enzymatic glycosylation of vascular endothelium leads to leakage of plasma proteins into vessel walls.
First drug given to diabetics with HTN or proteinuria? –> ACEi (e.g., enalapril) or ARB (e.g., valsartan).
Most common cause of chronic renal failure? –> diabetes mellitus.
BUN/Cr ratio in pre-, intra-, vs post-renal failure? –> >20 in pre-; <20 if not pre- –> FA for Step 1 had stratified this out as <15 for intra- and 15-20 for post-, but I’ve seen at least three 2CK NBME/CMS Qs where the diagnosis was acute tubular necrosis and the BUN/Cr was in the 16s or 17s. So I’ve learned to just tell students: >20 = pre-; if >20, you simply know it’s not pre-.
Fractional excretion of sodium (FeNa) in pre-/intra-/post-renal failure? –> need to know it’s <1% in pre-renal; >1% in intra-/post-renal –> the low FeNa in pre-renal is due to the PCT’s attempt to reabsorb Na (water follows sodium) in low-volume state (or in FMD, RAS).
Urine osmolality in pre-/intra-/post-renal failure? –> concentrated (high; >500 mOsm) in pre-; dilute (low; <350 mOsm) in intra-/-post.
When is pre-renal failure the answer apart from the BUN/Cr >20? –> CHF classically (decreased renal perfusion); can also be hypovolemia generally not in the acute setting; it’s to my observation that if the NBME/CMS Q mentions acute hypovolemia + no other information (i.e., does not mention BUN or Cr), the answer is acute tubular necrosis (intra-renal), not pre-renal. Pre-renal can also be the answer for contrast-nephropathy; regarding this point, contrast agents can cause either pre-renal (due to afferent arteriolar spasm) or intra-renal (direct nephrotoxicity); always give fluids to prevent (HY). The USMLE Q will sometimes give a presentation of pre-renal + ask the etiology, and the answer is “decreased glomerular filtration” (NBME).
Guy has MI + has low BP; NBME Q asks what is most likely to be seen (ask a bunch of reabsorption / secretion answers); answer = “increased potassium secretion” –> low-volume status leads to RAAS upregulation and distal renal K wasting.
When is intra-renal failure the answer? –> classically acute tubular necrosis (ATN) secondary to episodes of hypoxia at the kidney, usually due to blood loss (i.e, intra-operative requiring lots of blood, or traumatic exsanguination), or arrhythmia (i.e., patient had episode of VF and was resuscitated) –> vignette will mention one of the above scenarios and then tell you patient has acute oliguria +/- dark urine. They do not have to mention BUN, Cr, or muddy brown granular casts for ATN.
Other causes of intra-renal failure? –> drugs (i.e., gentamicin); rhabdomyolysis (myoglobin is nephrotoxic); contrast nephropathy.
Why does acute hypoxia cause acute tubular necrosis? –> proximal convoluted tubules have high concentrations of transporters (namely Na/K-ATPases) with high oxygen demand; also explains why diffuse cortical necrosis is classically associated with obstetric catastrophes.
Lab animal is given 100% nitrogen in dumb experiment; most likely part of the kidney to experience anoxic injury (they list everything) –> answer = “proximal tubule.”
Classic finding in urine with ATN? –> muddy brown granular casts; it should be noted that general “granular casts” are not specific to ATN. There’s an IM CMS Q with an elderly woman who has CVA tenderness + granular casts on U/A; answer is pyelo not ATN.
USMLE Q gives guy who has MI requiring resuscitation + subsequent oliguria; then they ask what you see on microscopic examination of the kidney; answer = “degenerating epithelial cells and dirty brown granular casts” or “necrosis of epithelial cells in proximal convoluted tubules.”
Electrolyte disturbance in ATN? –> first week is oliguric phase (hyperkalemia due to decreased filtration); weeks 2-3 are polyuric phase (hypokalemia due to increased kaliuresis from PCT cells not being able to reabsorb K yet) –> btw, kaliuresis means urination of K (great word if you want to feel sophisticated).
When is post-renal the answer? –> classically BPH or distal obstruction secondary to strictures or malignancy.
How does USMLE like to assess post-renal? –> classically will give you BPH + show you a pic of hydronephrosis (massively dilated kidney), then they’ll ask the most likely cause of this patient’s condition; answer = “increased Bowman capsule hydrostatic pressure,” or “increased tubular hydrostatic pressure.” This answer is on several NBMEs.
BPH Tx? –> alpha-1 blocker (e.g., tamsulosin, terazosin) and/or 5-alpha-reductase inhibitor (i.e., finasteride); patients may receive mono- or dual therapy.
Tx for prostatic adenocarcinoma? –> flutamide + leuprolide administered together (if the USMLE forces you to choose a sequence, pick flutamide then leuprolide, but in practice their administered together) à flutamide blocks androgen receptors; leuprolide is a GnRH receptor agonist (given continuously it shuts off LH/FSH secretion).
When is renal papillary necrosis the answer? –> classically in sickle cell; can also from drugs like NSAIDs; urine will be dark –> renal papillae in the medulla receive less blood flow, so small changes in the microvascular supply can lead to sloughing + necrosis of the medulla. You’ll be able to contrast this disorder from diffuse cortical necrosis and acute tubular necrosis because the latter two conditions, in the context of ischemia, are associated with massive, acute events.
