Teaching clinic: acute kidney injury

Question 1

Why dont have SGLT2 when fasting

Answer 1

Causes euglycemic ketoacidosis

Question 2

Prerenal, intrinsic renal problem/post renal for acute kidney injury

Answer 2

Prerenal
Intrinsic renal problem: glomerular (crescenteric IgA nephropathy, RPGN: 3 classes), tubulointerstitial, vascular/vasc endothelium
Post renal

Question 3

What are the possible causes for sudden decline in renal function?

Answer 3

• Immunotherapy associated AKI
• Diarrhea (can indicate underlying infection which cause kidney injury): causing dehydration (look for postural hypotension –> if patient edematous it cant be dehydration) –> hypovolemia (prerenal cause). Infection associated tubulointerstitial nephritis –> especially viral –> look for viral symptoms (normally will resolve by itself after virus is eradicated)
• Drugs: NSAIDs (acute tubulointerstitial nephritis/functional haemodynamic: blocks PG to relax afferent arteriole causing reduced renal perfusion), penicillin, rifampicin (thrombocytopenia with AKI –> stop drug), septrin (trimethoprim/sulfamethoxazole), TCM
• Decompensated cirrhosis with hepatorenal syndrome (will have ascites): more susceptible to prerenal causes
• On tacrolimus which is nephrotoxic: depends on exposure (which varies in everyone: depends on transportation/metabolism –> pharmacogenetics)

Question 4

Cause of immunotherapy mediated AKI

Answer 4

• Immune mediated tubulointerstitial nephritis
• Boost immune system to attack tumor cells: can be overreactive and attacks kidney parenchyma
• Histology: Some lymphocytes, neutrophils and eosinophils
• Timing is important (if more than 6 months ago not likely the main cause)

Question 5

Why may NSAIDs cause AKI?

Answer 5

↓ Renal prostaglandins synthesis for vasodilation which decreases renal blood flow and thus renal failure with Na+ retention

Question 6

Why does azathioprine causes myelosuppression in low dose?

Answer 6

TPMT (due to low enzyme that varies according to genetics)

However normally azathioprine causes myelosuppression in higher dosages
Calcineurin inhibitors have narrow therapeutic index hence have to monitor the blood levels

Question 7

Ix to be done

Answer 7

• Urinanalysis: RBC, protein
• Microscopy of urine: dysmorphic RBC
• Renal biopsy (after confirmation of RBC via urine microscopy): assess how much functional kidney is remaining (if all fibrotic giving immunosuppressants and steroids is of no use –> invites unnecessary infection): do light microscopy, immunofluorescence, electron microscopy
• Blood tests: anti GBM antibody, ANCA (PR3, NPO antigen)
• TPMT level: if excessive ie. >12 –> reduce the dosage –> the creatinine may return to normal

Question 8

PE of patient

Answer 8

• General examination: not cafe au lait (with creatinine at 100), pallor, pulse
• Ballotable kidneys: undiagnosed PKD, chronic uroobstructive cause
• Abnormal bruit –> more susceptible to minor fluctuations of dehydration/hypovolemia (don’t say renal bruit as cannot accurately iddentify): due to long standing HT, DM (ask if patient on smoking) –> if present be cautious of ACEi, ARB –> arrange doppler artery ASAP

Question 9

Causes of RBC+ in urinanalysis

Answer 9

• Renal: Glomerulonephritis (damage to the glomerular basement membrane): leakage through vascular epithelium –> bowmans capsule
• Postrenal: renal stone, tumor

Question 10

acute tubulointerstitial nephritis presentation

Answer 10

• Not proteinuria: as does not effect the podocyte/glomerular basement membrane
• Acute TIN with proteinuria: on NSAID (TIN with minimal change disease –> normal on light microscopy –> look at EM). Note on patient record: cannot take NSAID again.

Question 11

What to look for in heavy proteinuria?
What are the causes?

Answer 11

In heavy proteinuria: look for effacement of foot processes (electron microscopy) –> minimal change disease, membranous nephropathy, FSGS

Question 12

Cause and age distribution of acute GN (in 78 years old)

Answer 12

Anti GBM disease
Bimodal age: teenager, over 60

Requires treatment rapidly: causes rapid destruction (RPGN class 1)
Don’t be misled by normal creatinine levels

Question 13

Post sore throat 2 weeks with acute GN cause

Answer 13

PSGN

Question 14

Acute GN in this patient causes?

Answer 14

Anti GBM
ANCA associated GN (IF): PR3, NPO (more common in asians) antigen
Infection associated GN: Membranoproliferative GN (glomeruli shows central proliferation)

Question 15

Mx of anti-GBM

Answer 15

Plasmapharesis (wash out the Anti-GBM antibodies)

Question 16

Histology of anti-GBM

Answer 16

• Crescenteric GN: affecting more than 50% of glomeruli (RPGN)
• Linear staining of IgG (lining the continuous glomerular basement membrane)

Question 17

ANCA associated vasculitis histological features

Answer 17

• Necrotic lesions (necrotizing vasculitis)
• IF pattern: Pauci immune (not like lupus: local presence of Ig –> trigger complement activation) –> very little Ig deposition

Also known as pauci immune glomerulonephritis

Question 18

Lupus nephritis histological features

Answer 18

• Increased number of inflammatory cells
• Complement deposition (immune complex deposition disease: type 2 RPGN)
• Full house Ig deposition: GAM
• Deposition in subendothelial region

Question 19

igA nephropathy on histology

Answer 19

IgA and complement deposition
Differ from lupus nephritis: full house Ig deposition (GAM)

Question 20

Structures of glomerulus inside to out

Answer 20

vascular endothelium, capillary endothelium, glomerular basement membrane, podocytes, bowmans capsule

Question 21

glomerular disease causing subepithelial deposition of Ig?
Staining of Ig?
What further tests must be done?

Answer 21

• Membranous nephropathy (primary/secondary): abnormal Ig under podocytes affecting their function (flattening them)

Secondary membranous nephropathy
* Hep B associated
* SLE

Appearance of Ig staining
* Granular staining along the GBM

Requires staining with PLA2R (with primary membranous nephropathy)
THSD7A testing after PLA2R

Question 22

If linear staining on IF what is dx?

Answer 22

anti-GBM only