Renal Pathology

Question 1

What are the causes of pre-renal failure?

Answer 1

REDUCED RENAL PERFUSION:
Shock (septic, hypovolemic, cardiogenic, hemorrhagic)
DeH2O
Hemorrhage
Renal artery stenosis

Question 2

What are the causes of post-renal failure?

Answer 2

OBSTRUCTIVE:
Renal calculi - anywhere along the urinary tract
Prostate enlargement - benign/malig
Tumour - transitional cell carcinoma or mass effect from abdo mass

Question 3

Causes of acute intra-renal failure?

Answer 3

Acute-on-chronic kidney failure 
Glomerulonephritis 
ATN 
Tubulointerstitial disease
Vascular disease
Acute pyelonephritis
Myeloma

Question 4

What is glomerulonephritis?

Answer 4

Inflammatory injury to the renal glomeruli, mostly immune mediated

Question 5

Main features of glomerulonephritis?

Answer 5

Renal impairment - lower GFR, incr creatinine
Haematuria (RBC casts in urine)
Nephrotic syndrome - protein leak thru damaged GBM -> proteinuria, hypoalbuminaemia, peripheral oedema

Question 6

4 most important types of glomerulonephritis?

Answer 6

IgA nephropathy
Post-strep. glomerulonephritis
Membranous nephropathy
Minimal change disease

Question 7

Main features of IgA nephropathy?

Answer 7

Presents w haematuria and renal impairment, often a few days after URTI
H&E stain: mesangial hypercellularity, incr mesangial matrix formation
EM: electron dense (IgA) deposits in mesangium

Question 8

Main features of post-strep. glomerulonephritis?

Answer 8

Presents w haematuria and renal impairment
Occurs 1-4 weeks after strep pyogenes infection (pharyngitis/impetigo)
Mediated by IgG and C3 complement

Question 9

Main features of membranous nephropathy?

Answer 9

Presents w nephrotic syndrome
Deposition of immune complexes of epithelial side of the GBM
Immune complexes activate complement -> MACs form -> damage to GBM -> loss of -ve charge -> protein leakage
H&E: diffuse thickening of capillary walls w/out increased cellularity
EM: thickened GBM, e- dense immune complex deposits

Question 10

Main features of minimal change disease?

Answer 10

Most common in children
Idiopathic
H&E: normal
EM: fusion of base of podocyte foot processes
Negative immunofluorescence

Question 11

What is interstitial nephritis?

Answer 11

inflammation of connective tissue in which the glomeruli, tubules and blood vessels lie.

Question 12

Most common cause of interstitial nephritis?

Answer 12

Adverse drug reaction:
NSAIDs
antibiotics
diuretics
proton-pump inhibitors

also due to infection

Question 13

Presentation of interstitial nephritis?

Answer 13

Acute renal failure (sudden drop in urine output over 48 hrs.
Can also be a chronic asymptomatic condition that causes CKD and so a gradual decr GFR.

Question 14

Pathogenesis of interstitial nephritis?

Answer 14

ADR/infection -> infiltration of inflammatory cells into the interstitium.
More eosinophils, more likely a drug allergy
If mainly lymphocytes, indicates infection or kidney transplant rejection

Question 15

Causes of chronic renal failure?

Answer 15

diabetes
HTN
glomerulonephritis
Others: PKD, reflux nephropathy

Question 16

What is diabetic nephropathy?

Answer 16

One of the major microvascular complications of diabetes.
Manifests as progressive proteinuria.
Caused primarily by microangiopathy:
Formation of AGEs in endothelium leads to
thickening and concurrent weakening of vascular basement membranes.

Question 17

Key histological features of diabetic nephropathy?

Answer 17

Thickened GBM
Glomerulosclerosis - diffuse and global (w KW nodules in mesangium)
Mesangial expansion

Question 18

Pathophysiology of hyaline arteriolosclerosis?

Answer 18

Haemodynamic stress over time -> incr endothelial permeability -> depostion of plasma proteins in wall, incr ECM, smooth muscle atrophy
Additional proteins/matrix appears as a homogenous eosinophilic glassy material (hyaline) -> arteriole wall becomes thickened and narrowed
Made worse by systemic HTN

Question 19

Consequences of hyaline arteriolosclerosis?

Answer 19

If severe (eg in pts w systemic HTN) -> chronic ischemic atrophy of nephrons over time -> chronic renal failure