HY lecture notes:
Gold salts + sulfa drugs –> membranous glomerulonephritis –> nephrotic syndrome.
Aminoglycosides (e.g., gentamicin) –> acute tubular necrosis –> oliguria + dark urine with muddy brown granular casts.
Beta-lactams (e.g., nafcillin) + cephalosporins –> acute interstitial nephropathy (tubulointerstitial nephritis; interstitial nephritis) –> WBCs in the urine (eosinophils) +/- WBC casts –> the renal manifestation of an allergic reaction, and in turn, often associated with rash (but not mandatory in Qs).
Intersititial nephritis just means inflammation of the interstitium of the kidney, and whilst frequently due to allergic reaction from the above agents, can occur in the absence of allergy as well (NSAIDs). NSAIDs –> analgesic nephropathy –> due to ischemic damage from decreased renal blood flow.
Analgesic nephropathy is an umbella term which just means damage to the kidneys due to analgesics, but the type of damage may be interstitial nephropathy or renal papillary necrosis (ischemic damage; dark urine).
Patient is on beta-lactam or cephalosporin for several weeks –> WBCs in the urine –> answer = intersititial nephropathy.
Patient is on high-dose analgesics (NSAIDs, phenacetin) for several weeks, or lower dose analgesics for months to years –> peripheral edema –> answer = interstitial nephropathy (and because the etiology is analgesics, we can label it “analgesic nephropathy,” but the Dx is still interstitial nephritis). The edema is due to decreased renal blood flow –> kidney perceives fluid status as low –> compensatory increase in Na reabsorption through the PCT –> water follow sodium –> edema, FeNa <1%, and BUN/Cr >20.
Hepatitis B can also cause membranous glomerulonephritis.
Hepatitis C can cause membranoproliferative glomerulonephritis.
Child has edema, eyelid swelling, and/or ascites –> no blood in the urine –> minimal change disease (MCD; lipoid nephrosis). Usually caused by viral infection, but the vignette doesn’t have to mention that. MCD can also be caused by adults with Hodgkin lymphoma (cytokine effect).
Thrombotic thrombocytopenic purpura –> antibodies against ADAMTS13 –> pentad of thrombocytopenia + schistocytosis (hemolytic anemia) + hematuria + fever + neurologic signs. ADAMTS13 is normally responsible for cleaving vWF multimers –> in TTP, can’t cleave these multimers, so platelet clumps build up and can cause the shearing of RBCs (schistocytes).
Hemolytic uremic syndrome (HUS) –> due to EHEC shiga-like toxin (verotoxin) or shigella’s shiga toxin. Triad of thrombocytopenia + schistocytosis (hemolytic anemia) + hematuria. Toxin binds to GB3 receptors in the kidney (more receptors in kids than in adults). This causes leukocytes to bind to the endothelial cells –> endothelial damage –> platelets come in to heal damage –> platelets get consumed (thrombocytopenia). Toxin inactivates ADAMTS13, so the platelet clumps can’t get cleaved –> shear RBCs flying past in the renal microvasculature (same as TTP) –> schistocytosis.
Kid with sore throat. Red urine 1-3 DAYS later –> answer = IgA nephropathy
Kid with sore throat. Red urine 1-2 WEEKS later –> answer = post-streptococcal glomerulonephritis (PSGN).
Kid with yellow crusties (school sores) on the skin. Red urine 7 days later –> answer = PSGN (from impetigo). Can also occur from erysipelas and cellulitis caused by Group A Strep.
