Renal Flashcards
What are some causes of AKI? Categorise them
Prerenal:
- volume depletion
- reduced cardiac output
- systemic vasodilation => renal hypoperfusion
- drugs e.g. NSAIDs, ACE-i
Renal:
- acute tubular necrosis
- acute interstitial nephritis
- vascular
- glomerular
Postrenal:
- obstruction - stones, tumours, strictures, prostatic hypertrophy
What urine analysis findings can help investigate AKI?
🔹urine dipstick
- urinary tract infection: leucocytes +/- nitrites
- glomerulonephritis: haematuria + leucocytes
- acute interstitial nephritis: leucocytes by themselves
🔹microscopy, culture and sensitivity if any evidence of UTI on the urine dipstick
🔹protein:creatinine ratio if glomerulonephritis is suspected
What is the NICE criteria for diagnosis of AKI?
Any of the following:
🔹rise in serum Cr of >=26umol/L / 48hrs
🔹>50% inc in serum Cr over past 7 days
🔹UO < 0.5ml/kg/hr for >6 hrs
What is the RIFLE criteria? What is AKIN criteria?
RIFLE - Risk, Injury, Failure, Loss, End-stage renal disease
Uses serum Cr and UO to classify kidney injury
:::::
AKIN - uses stages 1-3 to classify AKI
What is the KDIGO classification?
Staging of AKI
1 = Cr x 1.5-1.9 or >26umol/L / 48 hrs
:: = UO < 0.5 ml/kg/hr > 6hrs
2 = Cr x 2.0-2.9
:: = UO < 0.5 ml/kg/hr >12hrs
3 = Cr x >3.0 baseline or >353.6 umol/L
:: = UO < 0.3 ml/kg/hr >24hr or anuria > 12hrs
What is the management of AKI?
Replace fluids
Hold nephrotoxics and review meds (NSAIDs, aminoglycosides, ACE-i, ARB, diuretics)
Treat underlying cause
What are some early and late clinical manifestations of CKD?
Early:
- fatigue (toxins, anaemia from reduced EPO)
- polyuria/nocturia
- HTN
- puffiness/swelling - fluid retention
Late:
- reduced UO
- fluid overload
- uraemia - N+V, anorexia, metallic taste, pruritis
- Neuro - poor concentration, fatigue, seizures, coma
- CVD
- anaemia
- bone and mineral disease - bone pain, fractures, renal osteodystrophy
- metabolic acidosis - Kussmaul breathing, confusion, lethargy
What causes anaemia in CKD?
- reduced EPO levels
- reduced erythropoiesis due to toxic effect of uraemia on bone marrow
- reduced iron absorption
- anorexia/nausea due to uraemia
- reduced red cell survival
- blood loss due to capillary fragility and poor platelet function
- stress ulceration => blood loss
What is the management of mineral bone disease in CKD?
aim to reduce phosphate and PTH levels
- reduce dietary intake
- phosphate binders
- vitamin D
- parathyroidectomy in some cases
How do ACE inhibitors have a renoprotective effect, particularly in diabetic nephropathy?
They cause dilation of the efferent glomerular arterioles, reducing glomerular capillary pressure and protecting the filtration barriers.