Teaching clinic: acute kidney injury Flashcards
Why dont have SGLT2 when fasting
Causes euglycemic ketoacidosis
Prerenal, intrinsic renal problem/post renal for acute kidney injury
Prerenal
Intrinsic renal problem: glomerular (crescenteric IgA nephropathy, RPGN: 3 classes), tubulointerstitial, vascular/vasc endothelium
Post renal
What are the possible causes for sudden decline in renal function?
- 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)
Cause of immunotherapy mediated AKI
- 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)
Why may NSAIDs cause AKI?
↓ Renal prostaglandins synthesis for vasodilation which decreases renal blood flow and thus renal failure with Na+ retention
Why does azathioprine causes myelosuppression in low dose?
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
Ix to be done
- 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
PE of patient
- 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
Causes of RBC+ in urinanalysis
- Renal: Glomerulonephritis (damage to the glomerular basement membrane): leakage through vascular epithelium –> bowmans capsule
- Postrenal: renal stone, tumor
acute tubulointerstitial nephritis presentation
- 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.
What to look for in heavy proteinuria?
What are the causes?
In heavy proteinuria: look for effacement of foot processes (electron microscopy) –> minimal change disease, membranous nephropathy, FSGS
Cause and age distribution of acute GN (in 78 years old)
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
Post sore throat 2 weeks with acute GN cause
PSGN
Acute GN in this patient causes?
Anti GBM
ANCA associated GN (IF): PR3, NPO (more common in asians) antigen
Infection associated GN: Membranoproliferative GN (glomeruli shows central proliferation)
Mx of anti-GBM
Plasmapharesis (wash out the Anti-GBM antibodies)
Histology of anti-GBM
- Crescenteric GN: affecting more than 50% of glomeruli (RPGN)
- Linear staining of IgG (lining the continuous glomerular basement membrane)
ANCA associated vasculitis histological features
- 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
Lupus nephritis histological features
- Increased number of inflammatory cells
- Complement deposition (immune complex deposition disease: type 2 RPGN)
- Full house Ig deposition: GAM
- Deposition in subendothelial region
igA nephropathy on histology
IgA and complement deposition
Differ from lupus nephritis: full house Ig deposition (GAM)
Structures of glomerulus inside to out
vascular endothelium, capillary endothelium, glomerular basement membrane, podocytes, bowmans capsule
glomerular disease causing subepithelial deposition of Ig?
Staining of Ig?
What further tests must be done?
- 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
If linear staining on IF what is dx?
anti-GBM only
