Glossary of Renal path, phys, pharm

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Microvillus transformation, foot process effacement --> MCD
What classes of drugs should be used to treat hypertension in:
Thiazide diuretic, beta-blocker, ACEi, ARB, aldo antagonist
What glomerular disease is hepatitis C associated with?
Membranoproliferative glomerulonephritis
What happens when you give an isotonic NaCl injection?
Remains almost entirely extracellular, causing an increase in the overall ECF volume.
What RTA is characterized by high urine pH, hypercalciuria, hypocitraturia, and calcium phosphate stones?
Type I RTA (Distal)
What substances can cause nephrotoxicity activity at:
Afferent arteriole
NSAIDs, sulfonamides
What would the urinalysis reveal in:
Pre-renal ARF
minimal protein
no cells or casts
Uosm > 500 (kidneys are functioning well)
FENa < 1 %

What are causes of Type I RTA?
Mutation in proton ATPase on alpha-intercalated cells
Mutation in carbonic anhydrase
Mutation in Cl-HCO3- exchanger on BL membrane
What classes of drugs should be used to treat hypertension in:
Beta blocker, ACEi, aldo antagonist
What happens when you give a hypertonic NaCl injection?
Some isotonic expansion of the ECF and some increase in osmolality, resulting in the extraction of water from the ICF.
What is the morphology of MPGN?
Large glomeruli, proliferation of mesangium and leukocytes. Lobular appearance. Thick GBM, often with double contour (subendothelial deposits)
What substances can cause nephrotoxicity activity at:
Metals, NSAIDs
What would the urinalysis reveal in:
Acute tubular necrosis
Mild protein
Uosm < 350
FENa > 1%

What classes of drugs should be used to treat hypertension in:
High CVD risk
Thiazide, beta blocker, ACEi, calcium channel blocker
What glomerular disease shows sausage-like immune complex deposits in mesangium and capillary loops?
What happens when a hypotonic NaCl injection is given?
Some isotonic increase in ECFV, proportional increases in ICFV and ECFV with reductions in ICF and ECF osmolalities.
What RTA is characterized by appropriately acidified urine, hyperchloremic acidosis but in acid balance, and bicarbonaturia when alkali is administered?
Type II RTA (Proximal)
What substances can cause nephrotoxicity activity at:
Proximal tubule
Metals, pigments (protein), antineoplastics (Cis-platin), antibacterials, cyclosporine, rampamycin
What would the urinalysis reveal in:
Acute interstitial necrosis
Mild protein
Uosm < 350
FENa > 1%

Collapsing glomerulonephropathy
What causes Type II RTA?
Impaired HCO3- reabsorption in proximal tubule (sometimes associated with Fanconi syndrome)
Caused by faulty Na-HCO3- cotransporter on BL membrane
What classes of drugs should be used to treat hypertension in:
Diabetes mellitus
Thiazide, beta-blocker, ACE-i, ARB, CCB
What entities can cause crescentic GN?
Anti-GBM (idiopathic or Goodpasture’s), immune complex (idiopathic, SLE, post-infx, HSP, IgA, MPGN), or pauci-immune (idiopathic, Wegener’s granulomatosis, or microscopic polyarteritis)
What happens when you give IV mannitol?
Stays in ECF, acts like NaCl. Used to relieve cerebral edema.
What substances can cause nephrotoxicity activity at:
Distal tubule
cis-platin, glycols (deposition)
What would the urinalysis reveal in:
Protein, blood
RBC casts
Uosm > 500 (this is weird)
FENa > 1%

Spikes and holes --> membranous GN
What are the two main features of pauci-immune GN?
Fibrinoid necrosis and crescents
What causes generalized edema? Localized?
Drop in plasma oncotic pressure. Increase in interstitial oncotic pressure.
What classes of drugs should be used to treat hypertension in:
Recurrent stroke prevention
Thiazide, ACEi
What happens if you give bicarb to someone with:
Distal RTA (Type I)
Proximal RTA (Type II)
Distal: serum HCO3- goes up, urine pH doesn't change much
Proximal: can't reabsorb any more HCO3-, so urine pH goes up, and serum HCO3- doesn't change much
What substances can cause nephrotoxicity activity at:
Collecting duct
Obstruction by anticholinergics, bromocriptine, quinolones, sulfonamides
What would the urinalysis reveal in:
Post renal ARF
minimal protein
varied microscopy
Uosm < 350
FENa > 1%

Spikes and holes --> membranous GN
How does CHF result in edema?
Reduced CO and systemic BP from left heart --> retention of NaCl and water. Expand vascular volume, mostly on venous side, increasing Pc.
How does toluene result in nephrotoxicity?
Causes myoglobinuria --> acute tubular necrosis
What are the two types of ANCA associated with?
C-ANCA - proteinase 3 – Wegener’s, occasionally idiopathic or MPA
P-ANCA – myeloperoxidase – MPA and idiopathic, occasionally Wegener’s
So basically this tells you nothing.
What classes of drugs should be used to treat hypertension in:
Benign prostatic hypertrophy
What is a lab hallmark of pre-renal ARF?
Elevated urea concentration out of proportion to creatinine elevation
because more filtrate is reabsorbed proximally, where urea is permeable
What RTA is characterized by acidic urine, hyperchloremic acidosis, and hyperkalemia?
Type IV - Hyporenin-Hypoaldosteronism

Spikes and holes (see red deposits in GBM) --> membranous GN
How does acetaminophen cause nephrotoxicity?
metabolite is a free radical that produces damaging protein adducts in liver and kidney
How does glomerulonephritis result in edema?
Retention of NaCl and water is primary (due to decreased GFR). Expand vascular space, resulting in (1) increased venous return from veins--> increased EDV --> increased BP --> inhibits renin release (2) Blood accumulates on venous side --> increased Pc --> transudation --> edema. Increased venous pressure stimulates release of ANP --> inhibit sodium reabsorption and promote diuresis
How does hypoaldosteronism lead to acidosis?
Hypoaldo --> hyperkalemia --> inhibits glutaminase and NH3 generation --> lack of buffer to accept protons --> backleak --> acidosis
What drugs can cause reduced perfusion, resulting in ARF?
NSAIDs, ACEi, cyclosporine
What is the mechanism of:
Aldosterone antagonist in cortical collecting duct
(Aldo's effects are to increase Na/K ATPase, K+ secretion, mitotic growth factor, upregulation of ENaC)
What is the therapy for pauci-immune GN?

Acute post strep GN
See neutrophils, some obliterated capillary lumina
How do aminoglycosides cause nephrotoxicity?
Magnesium and potassium wasting due to tubular damage
How do diuretics lead to metabolic alkalosis?
Loss of NaCl -> decreased EABV --> AII and aldo
AII--> increased HCO3- reabsorption in PT because there's a Cl- deficiency
Aldo --> increased H+ secretion in CCD
How does liver disease cause edema?
(1) cirrhosis – fibrosis leads to increased R --> increased Pc in acini --> ascites
(2) other liver disease – reduced production of albumin--> lowers oncotic pressure --> fluid leaks out of capillaries
What are the adverse reactions to:
Metabolic acidosis
What drugs can cause direct tubular toxicity, resulting in ARF?
Aminoglycosides, contrast, pigment, heavy metal
What kind of proteinuria is there in MCD?
Selective – albumin

Humps - pathognomonic for acute post strep GN
How does hyperaldosteronism lead to metabolic alkalosis?
Aldo stimulates intercalated cells to excrete H+
This is not Cl responsive!
How does the nephrotic syndrome result in edema?
Loss of urine protein > 3.5 g/day --> decreased plasma oncotic pressure --> fluid leaks into interstitium
How is the therapeutic index calculated?
What aldo blocker does not cause gynecomastia?
What drugs can cause allergic interstitial nephritis, leading to ARF?
Antibiotics, NSAIDs, phenytoin
What is the mechanism of MCD?
T-cell mediated and cytokines. Mutated nephrin.

IgA nephropathy
See mesangial hypercellularity, normal capillary loops on left.
Right - more severe, with some endocapillary and extracapillary proliferation (crescents)
How do you differentiate between MCD and other renal disorders?
Good response to corticosteroids.
How is the margin of safety calculated?
What drugs can cause tubular obstruction, resulting in ARF?
Acyclovir, sulfa
What is the mechanism of:
Loop diuretics
Inhibits Na/K/2Cl transporter in TALH

Double contours (not specific for IgA)
How does acetaminophen induce toxicity?
Metabolte free radical produces damaging protein adducts in liver and kidney.
How is urea handled in the nephron?
Freely filtered at glomerulus. 1/2 is passively reabsorbed in proximal tubule. The rest is impermeable except for the deepest part of the CD, where permeability is increased when ADH is present.
In what conditions is spironolactone used?
High aldo states (CHF, cirrhosis, hyperaldosteronism)
What are the mechanisms of decreased GFR in ATN?
Tubular cell damage
Obstruction from cell debris --> increased Pt
Loss of cell polarity and disruption of cell jxns --> backleak
Activation of tubuloglomerular feedback because of decreased proximal reabsorption of Na
Where are the deposits in membranous GN?

MPGN - see GBM thickening, abnormal lobulation of glomerulus, capillary lumens may be occluded
How do COX inhibitors cause toxicity?
Vasodilate afferent arteriole, compete with aldosterone --> hyperkalemia
How is creatinine handled in the nephron?
Freely filtered at glomerulus.. Not reabsorbed. Some is secreted. Estimates GFR because the secretion makes up for overestimation of plasma creatinine inherent in measurement methodology.
In what conditions are loop diuretics useful?
CHF, nephrotic syndrome, cirrhosis
What is the EM appearance of membranous GN?
Subepithelial deposits along GBM, separated by spikes

Double contours - in this case, it's MPGN, but it could also be IgA)
How do aminoglycosides and sulfonamides cause toxicity?
Aminoglycosides: magnesium and potassium wasting due to tubular damage
Sulfonamides: poor sulubility causes obstruction, also hypersensitivity vasculitis
How do you calculate GFR from creatinine levels?
GFR= (Ucr x urineflow)/Pcr
What are the ADRs of loop diuretics?
Hypokalemia, metabolic alkalosis, deafness
What is the IF appearance of membranous GN?
Granular deposits of Ig and complement along GBM

MPGN - sausage-shaped (semi-linear) deposits of IgG and C3
How is glucose handled in the nephron?
Freely filtered at glomerulus, actively reabsorbed in proximal tubule by a mechanism that has a transport maximum, which is about 370 mg/min --> glucose does not normally appear in urine if plasma glucose is normal
What are examples of loop diuretics?
Furosemide (Lasix), bumetanide, torsemide, ethacrynic acid
What kind of proteinuria is in FSGS?

MPGN - subendothelial and rare subEPIthelial deposits
Does FSGS recur after transplant?
Yes – suggests circulating factor.
What are three effects of PTH?
1) Promotes osteoclastic activity, mobilizing Ca2+ from bone
2) Increases activity of renal vitamin D3 1a-hydroxylase, which is required for synthesizing calcitriol, which increases intestinal reabsorption of Ca2+
3) Increases Ca2+ reabsorption from nephron and reduces the maximal transport for Pi, increasing Pi excretion
What is the mechanism of thiazide diuretics?
Inhibits Na/Cl transporter in distal convuluted tubule

Idiopathic pauci-immune
Fibrinoid necrosis without proliferation
Also crescents
Summarize the handling of Na+.
Oh goody.
Proximal tubule: 70% of Na is actively reabsorbed, Cl and water follow passively
Ascending limb of loop of Henle: 20% is reabsorbed by the Na/K/2Cl cotransport (impermeable to water)
Distal tubule: 5% Na is reabsorbed (Na/Cl cotransport), impermeable to water
Collecting duct: 3-5% reabsorbed by electrogenic Na channel pumps that are aldo regulated (ENaC). Variably permeable to water with regulation by ADH
If there is low aldo (from high blood pressure) – you get decreased Na reabsorption in CD
What are the ADRs of thiazides?
metabolic alkalosis,
gout (more UA absorbed with Na in proximal tubule under influence of AII),
glucose intolerance (hypokalemia impairs insulin release)
What is the morphology of FSGS?
Increased mesangial matrix, collapsed GBMs, deposition of hyaline masses and lipid droplets
IgM in the areas of hyalinosis

If you're thinking of either idiopathic pauci-immune GN or anti-GBM, what does this tell you?
This is anti-GBM, because you don't see immune complex deposits in pauci-immune.
What are examples of thiazides?
What are the effects of hypoaldosteronism?
Na loss, hypovolemia, decreased CO, decreased RBF
K+ retention, hyperkalemia, cardiac arrhythmias
H+ retention, metabolic acidosis
What is the morphology of acute post-strep GN?
LM- uniform increase in mesangial and endothelial cells, inflammatory infiltrate, thrombi in capillaries. Crescents – bad prognosis
EM – humps
IF – IgG and complement, subENDOthelial

Malignant hypertension
Top - Fibrous thrombosis
Bottom - Mucoid intimal hyperplasia and onion skinning
What is diabetes insipidus?
Either no synthesis of ADH (central) or ADH receptors in CD are resistant (nephrogenic)
Leads to inability to reabsorb water, leading to diuresis
What is the mechanism of acetozolamide?
Carbonic anhydrase inhibitor (decreased ability to exchange Na for H+) --> diuresis
What nephropathy occurs 1-2 days after a nonspecific upper respiratory infection?
Berger’s disease (IgA nephropathy)
How is H+ handled in the nephron?
Very low concentration in plasma. H+ is actively secreted by nephron, mostly in proximal tubule, 10% in CD. Most titrates HCO3- in tubular fluid, some reacts with ammonia, and some with other buffers (e.g. phosphates)
What are the ADRs of acetozolamide?
Metabolic acidosis (decreased HCO3- absorption)
What are the clinical manifestations of Alport’s syndrome?
Nephritis with nerve deafness and eye disorders, hematuria and proteinuria.
What are the clinical signs of diabetic nephropathy?
Microalbuminemia, grdual increase in proteinuria. Eventually Cr increases, renal failure. Retinopathy is indicative.
How is H+ secretion stimulated?
a) Respiratory acidosis leads to increased H+ secretion and therefore increases plasma HCO3- (renal compensation)
b) Aldo-increased Na reabsorption in CD causes H+ secretion to maintain electrical balance
c) Na+ reabsorption is balanced wither by passive K+ secretion or active H+ secretion. If K+ is in short supply, H+ secretion is stimulated.
What are other examples of K+ sparing diuretics?
(Block ENaC in collecting duct)
What are the pathological features of diabetic nephropathy?
Mesangial glomerulosclerosis - increased thickness in capillary walls, increase in mesangial matrix.
What is the morphology of Alport’s?
LM – segmental glomerular proliferation or sclerosis, increased mesagngial matrix. Foam cells. Tubular atrophy, interstitial fibrosis.
EM – thin BM, thickens with age. Basket weave appearance.
How can you tell the difference between metabolic and respiratory acid-base disturbances just by looking at H+ and bicarb?
If they change in same direction, it is RESPIRATORY
If they change in opposite directions, it is METABOLIC

If this also stained brown on silver stain, what would this be?
Diabetic nephropathy - this is nodular glomerulosclerosis, a Kimmelsteil-Wilson lesion. Notice also hypocellularity.
What are the ADRs of ACE-inhibitors?
be cautious with renal insufficiency (decreases GFR initially)
What are examples of ACE-inhibitors?
Captopril, lisinopril

What is this?
Diabetic nephropathy - thick GBM, foot process effacement secondary to hyperfiltration
When might renal compensation for metabolic alkalosis not be complete?
If there is accompanying severe volume depletion, because that will result in high also levels, which will result in increased H+ secretion.
How does autoregulation work?
1) Myogenic response in afferent arteriole – increased pressure opens stretch-activated Ca2+ channels, Ca enters smooth muscle cell, binds to calmodulin, activates MLCK, stimulates contraction, constricting arteriole
2) Tubuloglomerular feedback – macula densa monitors tubular fluid, signals to afferent and efferent arterioles through renin
What is the mechansim of Angiotensin II Receptor Blockers?
Blocks AI receptor of AII
Which amyloidosis is primary? Secondary?
AA -secondary
AL -primary

If this is also silver-negative, what is this?
Amyloidosis. This is also paler pink than Diabetic Nephropathy's nodular glomerulosclerosis.
What are examples of ARBs?
What is the effect of the sympathetic nervous system on the kidney?
Sympathetic only.
Alpha receptors – stimulate contraction, more of afferent than efferent (more muscle on aff)
Beta receptors – on JGA of afferent arterioles, release renin when stimulated, resulting AII constricts efferent arteriole, mainly. GFR is maintained while RBF is reduced

Amyloidosis w/congo red stain and polarized light.
In what conditions are beta blockers used?
Arrhythmias, angina, heart failure, high renin
What are the effects of angiotensin II?
Greater constriction of the efferent arteriole than afferent ‡ increase GFR
How can you distinguish btw AA and AL amyloidosis?
AA loses congo red affinity when treated with KMnO4.
Also, secondary immunostains with SAA in mesangium
What is the mechanism of action of beta blockers?
Decreased renin secretion
What stimulates the release of renin from the JGA?
a) Beta-1 receptors
b) Reduction in perfusion pressure (direct effect on JGA)
c) Reduction in Na+ delivery to macula densa (tubuloglomerular feedback)
What are the ADRs of beta blockers?
Negative dromotrope, inotrope, and chronotrope
Erectile dysfunction
What are the clinical features of adult polycystic disease?
Normal renal fxn until middle age, when they present with renal insufficiency, hematuria, flank pain, HTN.
Extrarenal: liver cysts, berry aneurysms in circle of Willis, mitral valve disease, colonic diverticula.
What is found in the urine in primary amyloidosis?
Light chains --> Bence-Jones proteinuria
What do elevated ANA levels indicate?
What is an example of a non-selective beta blocker?
What are its effects?
Decreases renin, CO, peripheral resistance (by decreasing SNS activity)
What is the histopathological appearance of the kidney in malignant hypertension?
Fibrinoid necrosis of arterioles (eosinophilic deposition in vessel walls) If inflammatory cells are present, it is necrotizing arteriolitis.
How do you distinguish between IgA and Type II SLE (mesangial lupus nephritis)?
EM looks the same (deposits in mesangium, mesangial proliferation).
IF - SLE stains for everything. IgA only IgA.
What is an example of a beta-1 blocker?
Metoprolol, atenolol
Less effect on bronchial constriction, vascular dilation
What type of pattern does immunofluorescence reveal in anti-GBM?
What are examples of alpha-1, beta adrenergic blockers?
Labetalol, carvedilol
Less effect on cardiac output and HR
What are the features of nephritic syndrome?
Proteinuria, hematuria, RBC casts, varying degrees of renal insufficiency and HTN
What is the most severe form of SLE?
Type III - diffuse proliferative GN
Neprhritic + nephrotic
What are the features of nephrotic syndrome?
Edema, severe proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia
What are the morphologic characteristics of Type III SLE?
Hypercellularity, crescents, fibrinoid necrosis. Double contours.
What is an example of an alpha-1 blocker, and what are its effects?
Prazosin, terazosin
Tamulosin (specific for prostate)
Vasodilation w/o reflex tachycardia
Used in BPH

Lupus - this is apparently a wire loop lesion.
What are examples of alpha-2 agonists? What are their effects?
Clonidine, alpha methyldopa
Stimulation of presynaptic alpha-2 receptors --> Decreased norepinephrine outflow from CV control centers in brain --> decreased peripheral autonomic tone
What are the most common causes of nephritic syndrome?
Acute post-strep glomerulonephritis, glomerular diseases (including SLE)

Wire loop lesion --> SLE
What are the ADRs of alpha 1 blockers?
First dose orthostasis
What are the most common causes of nephrotic syndrome?
Lipoid nephrosis (Minimal change disease) in children and elderly, membranous glomerulonephritis in adults

Wire loops in upper left hand corner --> SLE
What are the ADRs for alpha 2 agonists?
Sedation, rebound HTN if stopped, dry mouth
What are the features of Rapidly Progressive Glomerulonephritis (RPGN, a.k.a. crescentic GN)
Rapidly deteriorating renal function that accompanies glomerular injury. Nephritic urine sediment, renal failure. Accumulation of crescents (proliferation of parietal epithelial cells and migration of macrophages in Bowman space).

Oh my god, what is this?
SLE, Type V: there are deposits everywhere, thick GBM. Hematuria (RBC in urinary space)
SubEPIthelial deposits
What are examples of arterial dilators?
What are the causes of RPGN?
Idiopathic, multisystemic disease (vasculitis or Goodpasture), or follow post-strep.
What are ADRs for arterial dilators?
Na retention and edema --> use w/furosemide
Reflex tachycardia --> use w/B-blockers
Hydralazine may also lead to headache, N/V, lupus-liks syndrome
What are the clinical features of acute poststreptococcal GN?
Affects more children. Nephritic syndrome. Elevated antistreptolysin O titers, low serum complement.
What are the pathological features of acute poststrep GN?
Diffuse cellular proliferation and leukocytic infiltration--> hypercellularity
Electron microscopy shows subepithelial humps of Ag-Ab complexes
Granular deposits of immunoglobulins
What is the mechanism of CCBs?
Inhibits voltage-sensitive L-type channel on smooth muscle
What are examples of CCBs?
Dihydropyridine (nifedipine, amlodipine)
Non-dihydropyridine (verapamil, diltiazem)
What are the clinical features of MCD? (lipoid nephrosis)
Nephrotic syndrome. Caused by food allergy, medications, or hematologic malignancies.
What are ADRs of CCBs?
Dihydropyridines: headache, edema
non: negative inotropic, conduction delay, constipation w/verapamil
What is the proposed pathogenesis of MCD?
Lymphokine from T cells
Fusion of epithelial foot processes --> loss of polyanionic filter, leading to proteinuria
What is the mechanism and effect of reserpine?
Binds to central and peripheral adrenergic neuron storage vesicles --> antagonizes
What is the treatment of MCD?
Steroids --> complete recovery
What are the pathological findings of MCD?
Light- normal
Electron – loss of foot processes, but no electron-dense deposits in GBM
No immunofluorescence.
What are the potential side effects of alpha methyldopa?
- Hemolytic anemia
- Edema
- Impotence
- Sedation
- Increased prolactin -> lactation
What are the clinical and pathogenesis features of membranous GN?
Nephrotic syndrome, insidious onset. Usually idiopathic, but may be cause by infection, drugs, tumors, systemic disease.
Path: subepithelial immune disease deposits in GBMs ‡ damage capillary walls
What are the indications for nitroprusside?
Severe hypertensive crisis, aortic dissection
What are the adverse reactions associated with nitroprusside?
cyanide toxicity (lactic acidosis, arrhythmias, hypotension, hypoxia)
thiocyanate toxicity (weakness, disorientation, psychosis, muscle spasms)
Reflex tachycardia
What is the pathological appearance of the kidneys in membranous GN?
Swollen and pale grossly. Diffuse thickening of capillary walls.
Subepithelial deposits.
Granular pattern of Ig and complement
What are the clinical features of membranoproliferative GN?
Nephrotic or mixed nephritic/nephrotic syndrome.
Which calcium channel blocker is safe in CHF?
What are examples of thiazide diuretics?
Hydrochlorothiazide (HCTZ), chlorthalidone, metolazone (increasing in potency)
What is the pathogenesis of MPGN?
Type I: immune complex deposition in *subendothelium* and mesangium
Type II: C3 nephritic factor (an antibody against C3) with IgG antibody in serum. Dense deposits along glomerular and tubular BM
How does amiloride induce diuresis?
K+ sparing, directly inhibits Na+ reabsorption in collecting duct.
What is the pathological appearance in MPGN?
Mesangial proliferation, BM thickening, tram-tracking
EM: Type I subendothelial deposits of C3 and IgG
Type II: deposits of C3 in GBM
What are the clinical features of Focal Segmental Glomerulosclerosis?
Nephrotic syndrome, often with hematuria, HTN, impaired GFR, and non-selective proteinuria
What is the pathological appearance of FSGS?
Segmental sclerosis, hyalinization of glomeruli
EM: nonsclerotic regions show loss of foot processes. Sclerotic segments show increased mesangial matrix and mesangial deposits.
IgM and C3 deposits in sclerotic segments
What is the pathological appearance of Anti-GBM?
Crescents and fibrinoid necrosis
EM: no deposits, but GBM disruption
IF: linear pattern of Ig
What are the clinical features of Focal Proliferative GN?
May be primary or secondary to SLE, Goodpasture, SBE, or Wegener’s. May be subclinical or present with hematuria/proteinuria, occasionally nephrotic syndrome.
What are the clinical features of Berger disease (IgA nephropathy)?
Mild proteinuria. Recurrent hematuria. Occasional nephrotic syndrome. Usually follows a respiratory infection. Common cause of GN. Related to HSP.
What are the pathological features of Berger disease?
Variable. May be normal. Segmental proliferation, mesangial proliferation, or crescent formation.
EM: mesangial deposits
IF: mesangial IgA w/o complement
What are the clinical features of hereditary nephritis (Alport syndrome)?
Hereditary abnormality of collagen ‡ renal disease, deafness, ocular abnormalities (dislocated lens, corneal dystrophy, cataracts)
Hematuria, proteinuria, slowly progress to renal failure

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