Through the microscope : Glomerular diseases

This post will cover light microscopy(LM) , immunoflorescence(IF) and electron microscopy(EM) findings of some Glomerular diseases:-


LM = Normal appearing glomeruli

IF = Negetive

EM = Extensive foot process effacement(q)





LM = Segmental sclerosis in some but not all glomeruli

IF = Usually negetive (may have focal and weak mesangial C3 or IgM deposits)

EM = Focal foot process effacement, the degree of which depends on degree of proteinuria

Other EM findings of MCD/FSGS = Micovillous transformation of foot processes, endothelial cell edema, podocyte detachment and basement membrane wrinkling.

**Collapsing variant of FSGS(Q)

*It was first descibed in HIV patients(q) but its association is also seen with HBV, HCV, Parvovirus.

*LM = Main difference from usual FSGS is presence of segmental glomerular capillary collapse and podocyte proliferation ( in usual FSGS loop sclerosis and podocyte loss is prominent). Main pathogenesis of collapsing FSGS involves proliferation of podocytes.

*Collapsing FSGS have worst prognosis among all types of FSGS.





LM = Mesangial hypercellularity from focal to diffuse

IF = Predominat or  co-dominant IgA deposits in mesangium ( In HSP along with IgA deposits mild IgG and IgM deposits will also be seen)

EM = Show messangial deposits and occasionaly capillary loop subendothelial deposits may extend to GBM

NOTE : HSP mimics IgA pathology but it is a systemic disease which in addition to nephritis have skin rashes+ abdominal pain +arthritis

***IgA nephropathy is most common GLOMERULAR DISEASE worldwide with variable prognosis(30% develop ESRD) [ref : washington mannual of surgical pathology page 332/2nd ed].





LM = Thickening of capillary basement membrane while maintaining luminal patency. Silver stains show basement membrane ” spikes”

IF = Diffuse granular staining for IgG and C3 is present in glomerular basement membrane.

EM = Deposition is initialy subepithelial which become intramembranous as the disease progresses.

***Membranous GN is most common cause of nephrotic syndrome in ADULTS.

** An experimental model called HEYMANN NEPHRITIS  resembles Membranous GN pathologically.





LM = Wbc in glomeruli…neutro in acute and lympho/macrophase in chronic phase.

IF = Large granular IgG and C3 deposits along capillary loops.

EM = show charecteristic bell shaped subepithelial deposits calld as ” subepithelial hump”.

Note : Erythrogenic toxin type B is thought to be the target antigen that are deposited in the GBM.





Patients with MPGN can present with features of nephrotic and/or nephritic syndrome, and most patient have low C3 levels.

Type I is most common type.

LM = MPGN is a diffuse glomerulopathy with endocapillary proliferation and lobular accentuation. “Tram tracking” of basement membrane is seen in silver stains. These findings are more typical of type I.

IF = Diffuse granular staining for C3 is observed along glomerular capillary walls and messangium. 60% of type I have associated IgG and C1q positivity.

EM= MPGN type I shows ” subendothelial electron dense deposition” whereas type II is known as “dense deposit disease” as ribbon like electron dense deposits are seen along the capillaries, often replacing lamina densa. In MPGN type III both subendothelial and subepithelial deposits are seen.




So to summarise or what u need to remember is :-

*Foot process effacement is seen in :- minimal change disease ,FSGS , Membranous GN

*Collapsing FSGS have worst prognosis among all types of FSGS.

*Predominat or  co-dominant IgA deposits in mesangium = Mesangioproliferative GN

*Basement membrane spikes are seen in = Membranous GN

*Charecteristic bell shaped subepithelial deposits calld as ” subepithelial hump” Is seen in = Post infectious GN

*“Tram tracking” of basement membrane is seen in = MPGN TYPE I

*Dense deposit disease is known as =MPGN TYPE II

*Subepithelial deposits = Post infectious GN

*Subepithelial evolving to intramembranous = Membranous GN

*Subendothelial deposits = MPGN I

*Subendothelial and Subepithelial deposits = MPGN III

*Linear IgG staining along capillary basement membrane is seen in = Anti -GBM (Goodpasture,s disease) whereas Diffuse granular IgG and C3 staining is seen in Membranous GN.

This is not the end ……remaining is lupus nephritis/ dibetes/amyloidosis….will be updated soon


Renal tubular Acidosis (Frequently asked topic in various PG Entrance Examinations)

The word acidosis refers to the tendency for RTA to lower the blood’s pH. When the blood pH is below normal (7.35), this is called acidemia. The metabolic acidosis caused by RTA is a normal anion gap acidosis.

There are 4 types,only 3 are clinically important.Type 3 is Combined proximal and distal type,RTA type 3 is uncommon and seen only in children.

Type 1 (Distal RTA)-Distal RTA (dRTA) is the classical form of RTA, being the first described.

Underlying Defect-Selective deficiency in H+ secetion in Distal nephron by the alpha intercalated cells.

Electrolyte imbalance-Hypokalemic Hyperchloremic Metabolic acidosis

Despite acidosis urinary PH can not be acidified and is always above 5.5,

Etiology-Renal stone,amphotericin.cirrhosis and collagen vascular disease

Treatment-Potassium Citrate

Complication-Nephrolithiasis  (related to alkaline urine, hypercalciuria, and low urinary citrate)

Type ONE=stONE


Underlying Defect-Defect in proximal tubules’s ability to adequately reabsorb filtered HCO3 ions.

Electrolyte imbalance-Hypokalemic,Hyperchloremic Metabolic acidosis

The distal intercalated cells function normally, so the acidemia is less severe than dRTA and the urine can acidify to a pH of less than 5.3

Etiology-Carbonic Anhydrease inhibitors (acetazolamide,Diamox) ,Fanconi’s syndrome

Treatment-Potassium Citrate


Di-hard Fan of Type 2

Type 3 

In some patients, their RTA shares features of both Distal RTA and Proximal RTA.

A transient phenomenon in infants and children with dRTA (possibly in relation with some exogenous factor such as high salt intake) and is no longer observed.

This form of RTA has also been referred to as juvenile RTA.

Underlying Defect-inherited carbonic anhydrase II deficiency

Type 4-MC type RTA IN ADULTS

Underlying Defect-Hyporeninemic hypoaldosteronsim leads to defect in Na absorption,H+ and K+ excretion,Dcrease ammoniagenesis and Increase K+

Electrolyte Imbalance-Hyperkalemic,Hyperchloremic Metabolic acidosis

Etiology-MC found in Diabetic nephropathy,tubulointerstitial reanal disease and hypertensive nephrosclerosis.

Aldosterone deficiency (hypoaldosteronism)- Primary vs. hyporeninemic

Aldosterone resistance-
Drugs: NSAIDs, ACE inhibitors and ARBs, Eplerenone, Spironolactone, Trimethoprim, Pentamidine