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
RTA Type 4 (“HYPERkalemic”)
Def’n, Causes (3, incl 2 drugs), Labs (2)?
Abnormal Aldosterone production or response ->
*↓K + H EXCRETION *.
CAUSES:
- Dysfunction of ‘RAA Axis’ (ie due to Nephropathies)
- ACE Inhibitors
- K-Sparing Diuretics
LABS:
- HYPERkalemia
- Metabolic Acidosis (↓H EXCR =>↓NH3 EXCR)
Nephritic Sx
Proteinuria
Glomerulonephritis
Causes (2)?
CAUSES:
- Bacterial Endocarditis
- Wegener Granulomatosis
Acute Post-Streptococcal Glomerulonephritis
Locations Affected (2), Mech, H-S Type,
Micro Findings (LM + EM + IF),
Pres (Epi + CLUE), Labs (2), Urine (CLUE)
Prog?
- GBM
- Mesangium
MECH: IgG / IgM IC + C3 deposition along GBM and Mesangium.
Type 3 H-S.
FINDINGS:
- LM: enlarged + hypercellular glomeruli
- EM: subEPIthelial IC “humps”
- IF: “lumpy-bumpy” and “starry sky” granular appearance
PRES: MC in Children
- “Approx 2 wks after Group A Strep infection of skin or pharynx”
LABS:
- Anti-DNase B↑
- Complement levels↓
URINE:
- Dark “cola-colored” urine
PROG: Resolves spontaneously
RPGN
Def'n, Micro Findings (LM + IF), Antibodies, Seen In (3), Prog?
Nephritic Sx that progresses to Renal Failure in weeks.
FINDINGS:
- LM + IF: “Crescents”
AB:
- C-ANCA + P-ANCA
SEEN IN:
- Goodpasture Sx
- Wegener’s Granulomatosis
- Microscopic Polyangitis
PROG: Progresses to Renal Failure in WEEKS.
Diffuse Proliferative Glomerulonephritis
Locations (2), Mech, Causes (2),
Findings (LM + EM)?
- SubENDOthelial
- Intramembranous (sometimes)
MECH: IgG IC + C3 deposition.
CAUSES: (THINK: other 2 conditions in middle of venn diagram in FA)
- Membranoproliferative Glomerulonephritis
- SLE
FINDINGS:
- LM: “wire looping” of capillaries
- EM: subENDOthelial ICs
Berger’s IgA Nephropathy
Location, Mech,
Pres,
Seen In?
Mesangium.
MECH: IgA IC deposition.
PRES = often alongside a mucosal infection (ie URI or gastroenteritis).
SEEN IN:
- Henoch-Schonlein Purpura
Alport Sx
Location, Inher, Genetics, Mech (2 steps), Pres (2)?
Glom BM.
XR (MC).
Mutation -> Defective Type IV Collagen.
MECH:
Thin + split Glom BM -> Defective ability to FILTER BL.
PRES:
- Deafness
- Cataracts / ocular disturbances
Nephrotic Sx Proteinuria > 3.5 g / day
Location, Mech (2 = 2 Subtypes), Assoc (2), Micro Finding (CLUE), Labs / Pres (4), Urine (2), Comp (2)?
Glom BM.
MECH: Thickening of Glom BM:
- Due to IC deposition (Membranous types)
- Due to NEG (Diabetic Glomerulonephropathy)
ASSOC:
- Hep B + Hep C
- Systemic Amyloidosis
FINDINGS:
- Kimmelsteil-Wilson nodules in glom
- Preferential involvement of EFFERENT arterioles*
LABS / PRES:
- Loss of Antithrombin III (-> Hypercoag state, DIC)
- ↓Albumin (-> Pitting Edema)
- ↓Globulins (->↑risk of infection)
- ↑Lipids + Cholesterol (‘Fatty Casts’ in urine)
URINE:
- Proteinuria > 3.5 g / day
- Fatty Casts
COMP:
- Renovascular Htn
- 2ry Hyperaldosteronism
MPGN
Location, Def’n, Subtype Division?
Glom BM.
THICK Glom BM due to IC deposition.
Divided into 2 subtypes based on LOCATION of IC depositions.
MPGN Type 1
Location of IC Deposits,
Micro Finding?
SUBENDOTHELIAL IC deposits.
FINDINGS:
- “Tram-Track” appearance of Glom BM
MPGN Type 2
Location of IC Deposits, Assoc,
Micro Finding?
INTRAMEMB IC deposits.
ASSOC:
- C3 Nephritic Factor
(stabilizes C3 Convertase -> OVERACTIVE Complement ->↓serum C3)
FINDINGS:
- “Dense deposits”
Membranous Nephropathy
Def’n, Assoc (4),
Micro Findings (EM), Pres (Epi), Antibodies
Comp?
THICK Glom BM due to IC deposition.
ASSOC:
- Infections (ie Hep B + Hep C)
- SLE
- Solid tumors
- Drugs (ie NSAIDS + Penicillamine)
FINDINGS:
- EM: “spike and dome” appearance of IC deposits
PRES: Caucasion Adults
AB:
COMP: (poor response to steroid therapy)
- May progress to Chronic Kidney Disease
Diabetic Glomerulonephropathy
Mech / Locations (2 NEG pathways), Micro Findings (CLUE)?
MECH:
- NEG of Vascular BM -> E.A + Mesangial Hyaline Sclerosis
- >↑GFR -> Hyperfiltration - NEG of Glom BM -> Thickening +↑Permeability (->Microalbuminuria)
FINDINGS:
- Kimmelstiel-Wilson nodules
Focal Segmental Glomerulosclerosis
Path (2), Assoc (6)
Micro Findings (EM), Pres (Epi),
Comp?
PATH:
- Hyalinosis
- Segmental Sclerosis
ASSOC:
- Massive Obesity
- Sickle Cell Disease
- Chronic Kidney Disease
- HIV
- Heroin abuse
- Interferon treatment
FINDINGS:
- EM: Foot process effacement
PRES: African-American or Hispanic Adults
COMP: (inconsistent response to steroid therapy)
- May progress to Chronic Kidney Disease
Amyloidosis
Location, Def'n, Assoc, Micro Findings (LM)?
Mesangium.
Amyloid deposits in mesangium.
ASSOC:
- Chronic conditions (ie RA, TB, Multiple Myeloma)
FINDINGS:
- LM: Apple-Green birefringence on Congo Red stain
Minimal Change Disease (Lipid Nephrosis)
Location, Def’n, Mech (of Proteinuria), Assoc (2),
Micro Findings (EM), Pres (Epi),
RX?
Glom BM.
Glom BM POLYANION loss.
MECH:
Grade 1 glom injury = Selective Proteinuria = Albuminuria.
ASSOC:
- Recent infection or immune stimulus (eg immunization)
- Hodgkin Lymphoma (cytokine-mediated damage from T cells)
FINDINGS:
- EM: Foot process effacement
PRES: Children
RX = Corticosteroids (excellent response)
Kidney Stones
Seen In, Pres (3)?
SEEN IN:
- MEN I
PRES:
- Unilateral flank tenderness
- Colicky pain radiating to groin
- Hematuria
Ca Oxalate Kidney Stones
Causes / Assoc (5)?
CAUSES / ASSOC:
- Hypercalciuria
- RTA Type 1
- Crohn Disease
- Vitamin C abuse
- Ethylene Glycol poisoning
UT Obstruction
Causes (4), Comp (2)?
CAUSES:
- Injury to Ureter
- Renal Stones
- BPH
- Cervical Cancer
COMP:
- Hydronephrosis
- Pyelonephritis
Renal Failure
Def’n, Comp (* “MAD HUNGER”)?
Inability to make urine and excrete nitrogenous wastes.
COMP:
- Metabolic Acidosis
- Dyslipidemia (esp↑triglycerides)
- Hyperkalemia, Hyperphosphatemia, HYPOcalcemia.
Hyperaldosteronism, Hyperparathyroidism.
- Uremia
- Na / H20 Retention
- Growth Retardation / Devel Delay (in children)
- Erythropoietin synthesis failure
- Renal Osteodystrophy
Acute Renal Failure
Def’n, Labs (4)?
Acute / abrupt decline in renal function (within days).
LABS:
- ↓GFR and
- ↑BUN + Creatinine
- Azotemia
- Oliguria
Hydronephrosis
Location, Path, Causes (3)?
Renal Pelvices + Calyces PROXIMAL to site of pathology.
PATH: Distension / dilation -> Compression Atrophy.
** Only impairs renal function if bilateral or if patient only has 1 kidney **
CAUSES:
- UT obstruction
- Vesicoureteral reflux
- Retroperitoneal fibrosis
Renal Oncocytoma
Def’n,
Micro Finding,
RX?
Benign epithelial cell tumor of kidney tubules.
FINDINGS:
- Large eosinophilic cells with abundant mitochondria, round nuclei and
NO perinuclear clearing.
RX = Nephrectomy
Renal Cell Carcinoma (RCC)
Def’n, Inher (General), Genetics, Assoc (4),
Micro Findings, Pres (Epi + 4), Labs, Urine,
Mets, Rx (2)?
Malignant epithelial cell tumor arising from kidney tubules.
Sporadic or Inherited.
Deletion of VHL gene.
ASSOC:
- Obesity
- Smoking
- Paraneoplastic Sx: Ectopic ACTH, EPO, Prolactin + PTH
- Varicocele (L-sided RCC)
FINDINGS:
- Polygonal CLEAR cells, filled with accumulated carbs + lipids
PRES: Male 50-70 yrs
- Fever
- Weight loss
- Flank pain
- Palpable mass
LABS:
- 2ry Polycythemia
URINE:
- Hematuria
METS: Invades IVC -> Hematogenous spread.
RX:
- Resection (if localized)
- Immunotherapy (if metastatic)
Renovascular Htn
Causes (3)?
CAUSES:
- Renal art stenosis
- Nephrotic Sx
- Chronic Renal Failure
Transitional Cell Carcinoma
MC Location, Assoc (4: * “P SAC” *), Prognosis?
MC location = Bladder.
ASSOC:
- Phenacetin
- Smoking
- Aniline dyes (industrial, precursor to polyurethane)
- Cyclophosphamide
PROG: Tumors often multifocal and tend to recur.
Squamous Cell Carcinoma of Bladder
Mech (4 steps), RF (4), Pres?
MECH:
Chronic bladder irritation -> Squamous METAPLASIA ->
Squamous DYSPLASIA -> Squamous Carcinoma.
RF:
- Smoking
- Chronic Cystitis
- Chronic Kidney Stones
- Schistosoma haemotobium infection (Middle East)
PRES:
- Painless hematuria
Wilms Tumor (Nephroblastoma)
Def’n, Genetics, Assoc (2), Composition (3),
Pres (Epi + 2), Urine?
Malignant renal tumor.
WT1 or WT2 (tumor suppressor genes, chr 11) “loss of function”
mutations.
ASSOC:
- WAGR Sx
- Beckwith-Wiedemann Sx
COMPOSITION:
- EMBRYONIC glom / tubular structures
- ‘Blastema’ (immature kidney mesenchyme)
- Stromal cells
PRES: Children 2-4 yrs
- HUGE palpable flank mass and/or Hematuria
- Htn (Renin)
URINE:
- Hematuria
WAGR Sx
Pres (* “WAGR” *)?
PRES:
- Wilms Tumor
- Aniridia (absence of iris)
- Genitourinary malformation
- Retardation
