Glomerular Dz Flashcards
Objectives
Nephrotic Syndrome Epidemiology
- 15x more common in kids than adults
- In children, 2-7 cases per 100,000
- MCC = Minimal Change Disease (lipoid nephrosis)
Nephrotic Syndrome risk factors
- Because nephrotic syndrome is not itself a disease, risk factors for it are diseases that cause it except when it is idiopathic
Nephrotic Syndrome Etiologies
- MCD (lipoid nephrosis)
- Diabetes mellitus
- Membranous nephropathy: hepatitis B, gold, penicillamine, syphilis, carcinomas
- SLE
- Focal glomerulosclerosis: heroin, AIDS
- Amyloidosis
Nephrotic Syndrome signs and symptoms
- Generalized edema
- Heavy proteinuria (>3.5 gm/24 hrs)
- Foamy urine
- Hypoalbuminemia
- Hyperlipidemia
- Lipiduria
- NO HTN (unless pre-existing)
- Hypercoaguability (loss of anticoag proteins in the urine e.g. prot C, prot S)
- PE,DVT
- Infections (loss of immunoglobulins in urine)
- More susceptible to bacterial infections
Maltese cross
- oval fat bodies
- seen from lipiduria

Nephrotic Syndrome complications
- Cardiovascular ds bc of hyperlipidemia
- atherlosclerosis
- DVT, PE bc of hypercoaguability
- Infections bc of hypoimmunoglobulinemia
- Especially bacterial
Nephrotic Syndrome Dx
- Easy to diagnose nephrotic syndrome, important thing is to find cause
- H&P
- UA, 24 hr urine collection
- make sure min of 3.5g/min
- Renal biopsy
Nephrotic Syndrome management
- Steroids most useful for MCD or SLE
- Treat underlying cause
- General measures
- control HTN if present
- early treatment of infection
- So it doesn’t turn into pyelonephritis
- avoid nephrotoxic agents
- NSAIDs
- Aminoglycosides
- contrast dye
- If must use it, consult radiologist for alternative option
Nephrotic Syndrome prevention
- ACE inhibitors or ARBs in DM with HTN
- Microalbuminuria is 1st sign of DMà nephrotic syndrome
- Can be Idiopathic
Diabetic Nephropathy Epidemiology
- MCC of end stage kidney disease in the US
- ¼ of diabetics have it
- Onset is usually 10-15 years after dx
Diabetic Nephropathy Risk Factors
- inc. incidence of nephropathy in DM patients with
- Poor glucose control
- Uncontrolled HTN
- Type 1 DM, with onset < 20yo
- Past or current smoking
- FH of diabetic nephropathy
Diabetic Nephropathy Pathophys
- long-standing poorly controlled BG → changes in nephrons
- 1st efferent arteriole constriction and afferent arteriole dilation → glomerular capillary HTN and hyperfiltration
- gradually changes to hypofiltration
- concurrently, there are changes within glomerulus
- BM thickening
- widening of podocyte slit membranes
- inc. number of mesangial cells and↑ mesangial matrix
- matrix invades glomerular capillaries and produces deposits (Kimmelstiel-Wilson nodules)à true cause of complications
- mesangial cells and matrix progressively expand and consume entire glomerulus, shutting off filtration

Diabetic Nephropathy Signs and symptoms
- MC 1st symptom is nocturia
- 1st sign is microalbuminuria
- fatigue, malaise, anorexia
- HA
- N&V
- urinary frequency
- pruritis
- edema
Diabetic Nephropathy Dx
- Screen pts with Type 1 after 5 years
- Screen pts with Type 2 upon dx
- Results + in 2 of 3 tests in a 3- to 6-month period confirm dx
- transient elevations of microalbuminuria can be caused by exercise, UTI, hyperglycemia, febrile illness, severe HTN, or HF
- 3 ways to screen for albuminuria
- albumin-to-creatinine ratio on a spot urine test
- ratio >30 mg albumin/1 g creatinine is considered increased
- timed collection (e.g., 10 hrs overnight)
- 24-hour urine collection
- Normal <30 mg/24 hr
- Microalbuminuria 30–299 mg/24 hr
- Macroalbuminuria >300 mg/24 hr
- albumin-to-creatinine ratio on a spot urine test
Diabetic Nephropathy management
- Can progress to overtly nephrotic levels of proteinuria (>3.5 grams/24 hr)
- Main goal is to slow progression
- Control blood sugar HgbA1c <7
- Control HTN <130/80
- ACEI or ARB
- Low salt diet
**Diabetic nephropathy is not yet renal failure
**The goal is to slow the progression
Glomerulonephritis (Nephritic syndrome) incidence and risk factors
- True incidence of biopsy-proven GN unknown
- Because it is a syndrome and not a single disease entity, risk factors are diseases known to cause it
Glomerulonephritis Etiologies
- Post-infectious: MCC = strep throat
- Autoimmune response to presence of Strep, which ends up attacking the kidney
- Membranoproliferative GN
- SLE
- IgA nephropathy
- Goodpasture’s syndrome
- Vasculitides: PAN, Wegener’s granulomatosis
- Henoch-Schonlein purpura, HUS (E. coli)
- Assoc with endocarditis and visceral abscesses
Glomerulonephritis Acute vs. Chronic
- Almost any cause of acute may become chronic but post-infectious is almost always acute and self-limited
- Chronic GN is a major cause of CRF
Glomerulonephritis Pathophys
- Inflammaiton of glomerulus often due to autoimmune damage
- Damaged glomerulus allows leakage of red blood cells, protein, initiation of RAA which leads to fluid retention and HTN
Glomerulonephritis signs and symptoms
- mild edema
- moderate proteinuria
- HTN
- Will always cause
- hematuria (brown) and RBC casts
- Blood can also be grey due to iron which is reduced; also called “smokey” urine
- Having casts in urine is also called cylinduria
RBC casts=..?
glomerulonephritis

Glomerulonephritis Dx
- H&P
- UA, 24 hr urine collection
- Renal biopsy
- cANCA for Wegener’
Glomerulonephritis management
- Steroids, cytotoxic drugs in SLE, Goodpasture’s, Wegener’s
- Treat underlying cause
- General measures:
- control HTN
- early treatment of infection
- avoid nephrotoxic agents
Hypertensive nephrosclerosis
- Intimal thickening and luminal narrowing of large and small renal arteries and glomerular arterioles
- Global and focal segmental sclerosis of glomeruli

Hypertensive nephrosclerosis Demographics
- Associated with chronic HTN, especially if very high
- More common in Blacks, even at similar BP to whites
- More common in DM and others with underlying kidney dz
Hypertensive nephrosclerosis Signs and Symptoms
- Typically present with long history of uncontrolled HTN
- Slowly progressive increase in BUN, creatinine
- Mild proteinuria with benign urine sediment
- NOT RBC
- NOT RBC CASTS
- If they are seen then called “active urine sediment”
- Hyperuricemia
- May progress to ESRD
Hypertensive nephrosclerosis Dx
- Cinical diagnosis, no specific tests
- Renal biopsy is diagnostic but rarely needed
Hypertensive nephrosclerosis management
- CONTROL BP!!!!!
- MAY slow progression
- Damage may already be done
- BUT in AASK trial, pts with lower BPs did not have significantly better outcomes
AND
- ACEIs were only renoprotective in pts who initially presented with proteinuria