RENAL Flashcards
Cellular “crescents” in Bowman Capsule
RPGN
“Horseshoe” Kidney
Seen In?
Turner Sx
“Linear IgG deposition” on glom BM
Goodpasture Sx
Anti-BM ab -> Necrotizing glomerulonephritis
“Lumpy bumpy” appearance of glom on IF
Acute Post-Streptococcal Glomerulonephritis
Immune complex deposition of IgG + C3b
“Nodular hyaline deposits” in glom
Kimmelstiel-Wilson nodules: acellular nodules in glom
SEEN IN:
- Diabetic Nephropathy
“Podocyte fusion / effacement” on EM (2)
- Focal Segmental Glomerulosclerosis
- Minimal Change Disease (CHILD with Nephrotic Sx)
- “Spikes” on BM (irregular dense deposits)
- “Dome-like” subepithelial deposits
Membranous Glomerulonephritis
“Shrunken Kidneys” on U/S
Medullary Cystic Disease
“Thyroid-like appearance” of Kidney
Chronic Bacterial Pyelonephritis
“Tram-track” (ie double contour) appearance of capillary loops of BM on LM
Membranoproliferative Glomerulonephritis
“Wire loop” appearance of glomerular capillaries on LM
Lupus Nephropathy / Nephritis
(Thickened capillary BM due to IC deposition.
Type 3 H-S.)
- Male, 50-70 years, obese + smoker
- Von Hippel-Lindau Sx
Renal Cell Carcinoma
EXCESS Na / H2O Retention
Conseq (3)?
CONSEQ:
- Htn
- Pulm Edema
- CHF
Edematous States (4)
- Pulm Edema
- CHF
- Cirrhosis
- Nephrotic Sx
Edema of Renal Origin
Pres?
PRES = Usually first manifests around eyes + face
Normal Pregnancy
Urine (2)?
URINE:
- Glucosuria
- Aminoaciduria
Hartnup Disease
Inher, Mech (3 steps), Pres, Urine, Rx (2)?
AR.
MECH:
↓Neutral A.A Transporters in PCT ->↓A.A REABS from gut ->
Neutral Aminoaciduria.
PRES:
- Pellagra-like
URINE:
- Neutral Aminoaciduria
RX:
- High Protein diet
- Nicotinic acid
Fanconi Sx (PCT reabsorption defect)
Mech (↑Excr of 4), Causes (3), Pres (5)?
PCT reabs defect ->
↑EXCRETION of Glucose, A.A, HCO3 + Phosphate.
CAUSES:
- Hereditary defects (ie Wilson Disease)
- Ischemia
- Drugs (nephrotoxic)
PRES:
- Polyuria
- Proximal Renal Tubular Acidosis (Type 2)
- Electrolyte imbalances
- Growth failure
- Hypophosphatemic Rickets
Bartter Sx
Def’n, Inher, Labs (3)?
TAL reabsorption defect affecting Na/K/2 Cl Cotransporter.
AR.
LABS:
- Metabolic Alkalosis
- HYPOkalemia
- HYPERcalciuria
Gitelman Sx
Def’n, Inher, Pres?
DCT reabsorption defect of NaCl.
AR.
PRES = Same as Bartter Sx (Metabolic Alkalosis + HYPOkalemia), however WITHOUT Hypercalciuria and less severe.
Liddle Sx
Def’n, Mech, Pres (4), RX?
↑Na reabs in Collecting Duct.
MECH:↑activity of Na channel.
PRES:
- Htn
- Metabolic Alkalosis
- HYPOkalemia
- ↓Aldosterone (THINK: Aldosterone not needed if Na reabs is already increased.)
RX:
- Amiloride (inhibits Na channel in Collecting Duct)
Renal Tubular Acidosis (RTA)
Mech, Path, Labs, RX (3 main lines)?
MECH: Kidneys not appropriately acidifying urine.
PATH: Normal AG Metabolic Acidosis
LABS: HYPERkalemia
RX: Correction of pH + electrolyte imbalances (esp HYPERkalemia)
- Alkaline agents
- Electrolytes
- K restriction / K-wasting Diuretics
RTA Type 1 (Urine pH > 5.5) RARE
Def’n, Mech (2), Causes (4), Conseq (3), Labs (2), Urine?
Defect in H/K Antiporter of a-intercalated cells in Distal Tubule.
MECH:
- No H SECR -> New HCO3 can’t be generated -> Metabolic Acidosis.
- No K REABS -> HYPOkalemia.
CAUSES:
- Congenital anomalies -> OBSTRUCTION of urinary tract
- Amphotericin B Toxicity
- Analgesic Nephropathy
- Multiple Myeloma (light chain)
CONSEQ:
- ↑Urine pH > 5.5 (b/c no H excr)
- ↑Bone turnover (bone BUFFERS acid in bl + releases Ca Phosphate)
- ↑risk of Ca Phosphate Kidney Stones (for 2 above reasons)
LABS:
- HCO3↓(
RTA Type 2 RARE
Def’n, Mech (General -> 2 Conseq), Causes (3),
Urine (2: pH + excr),
Conseq?
Defect in PCT HCO3 REABS.
MECH: ↑HCO3 in tubular fluid (TF):
- > ↑HCO3 EXCRETION in urine -> Metabolic Acidosis.
- > TF more negatively charged -> Attracts K -> Hypokalemia.
CAUSES:
- Drugs / Chemicals toxic to PCT (ie Aminoglycosides, Expired Tetracycline, Lead)
- Fanconi Sx
- Light-Chain Multiple Myeloma
URINE:
- pH > 7 if plasma HCO3 normal ; pH