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NP25 Nephrology

Parenchymal Kidney Diseases

HIV-Associated Renal Disease


1. direct nephrotoxic effect of HIV infection, antiretroviral drugs (e.g. tenofovir, indinavir), and
other drugs used to treat HIV-associated infections
2. HIV-associated nephropathy
histology: focal and segmental glomerular collapse with mesangial sclerosis; collapsing FSGS
tubular cystic dilation and tubulo-reticular inclusions
clinical features: predominant in African American men, heavy proteinuria, progressive
renal insufficiency
prognosis: kidney failure within 1 yr without treatment
therapy: short-term, high dose steroids, ACEI, HAART
Infective Endocarditis
manifests as mild form of acute nephritic syndrome with decreased serum complement
S. aureus is most common infecting agent
treatment with appropriate antibiotics usually resolves GN
Hepatitis B
can result in membranous nephropathy, polyarteritis nodosa, membranoproliferative GN
Hepatitis C
can result in membranoproliferative GN, cryoglobulinemia, and membranous nephropathy
Syphilis
can result in membranous GN

Tubulointerstitial Disease
TUBULOINTERSTITIAL NEPHRITIS
Definition
cellular infiltrates affecting primarily the renal interstitium and tubular cells
functional tubule defects are disproportionately greater than the decrease in GFR
classified as acute or chronic
Signs and Symptoms
manifestation of disease depends on site of tubule affected
1. proximal tubule (e.g. multiple myeloma, heavy metals)
Fanconi syndrome: decreased reabsorption in proximal tubule causing glycosuria,
aminoaciduria, phosphaturia, hypouricemia
proximal RTA (decreased bicarbonate absorption): Type II RTA
2. distal tubule (e.g. amyloidosis, obstruction)
distal RTA (Type I RTA), usually hypokalemic
Na+-wasting nephropathy
hyperkalemia leading to type IV RTA (where reduced renal bicarbonate production is
caused by hyperkalemia)
3. collecting duct (e.g. sickle cell anemia, analgesics, PCKD)
urinary concentrating defect leading to mild nephrogenic DI
polyuria
1. ACUTE TUBULOINTERSTITIAL NEPHRITIS
Definition
rapid (days to weeks) decline in renal function
10-20% of all AKI
Etiology
hypersensitivity
1. antibiotics: -lactams, sulfonamides, rifampin, quinolones, cephalosporins
2. other: NSAIDs, allopurinol, furosemide, thiazides, triamterene, PPIs, acyclovir, phenytoin,
cimetidine
infections
bacterial pyelonephritis, Streptococcus, brucellosis, Legionella, CMV, EBV, toxoplasmosis,
leptospirosis
immune
SLE, acute allograft rejection, Sjgrens syndrome, sarcoidosis, mixed essential
cryoglobulinemia
idiopathic
Pathophysiology
acute inflammatory cell infiltrates into renal interstitium

Essential Med Notes 2015