Renal Flashcards
List common causes of acute kidney injury
Prerenal – hypovolemia, decreased CO, impaired renal autoregulation (NSAIDs, ACEi/ARB, cyclosporine)
Intrinsic – acute glomerulonephritis, vasculitis, malignant hypertension
Postrenal – bladder outlet obstruction, bilateral pelviureteric obstruction
List investigations to do for suspected AKI
Urine dipstick
Daily FBC, U&Es, LFTs, bone profile, CRP
Urine PCR, urine MC+S, USS KUB
Describe the management of an AKI
Discontinue nephrotoxic agents
Ensure volume status & perfusion pressure – IV fluids/diuretics, aim for euvolemia
Monitor urine output & daily bloods
Avoid hyperglycaemia
Treat underlying cause
Refer to specialist for consideration of RRT & consider ICU admission
List presenting symptoms of nephrotic syndrome
Oedema
Albumin <30
Urine PCR > 350 (more than 3.5 grams of protein in 24 hours)
Describe the management of glomerulonephritis
MDT approach depending on underlying diagnosis
ACEi/ARB for proteinuria
Control BP
Salt and water restriction if fluid overload
Diuretics for fluid overload
Consider therapeutic LMWH, if hypoalbuminaemic
Statins
Immunosuppressive therapy – specific to the cause
Invasive therapy
Describe the treatment for diabetic nephropathy
Intensive DM control
BP < 130/80, use ACEi/ARB
Sodium restriction <2g/day
Statins to reduce CV risk
Describe the management of chronic kidney disease
Treat underlying disease
Reduce CVS risk – statin, BP control, control diabetes, weight loss, exercise, stop smoking
Reduce progression of CKD – reduce proteinuria: ACEi/ARB
Prevent/treat complications of CKD – low phosphate/low K+ diet, phosphate binders, IV iron/folate/vit B12 replacement
Plan for future – RRT, home care team input, transplant
List complications of CKD
Anaemia of chronic kidney disease
Mineral & bone disease
Secondary & tertiary hyperparathyroidism
CVS disease
Electrolyte disturbances, fluid overload, metabolic acidosis, uraemic pericarditis, uraemic encephalopathy
Describe the pathophysiology of mineral bone disease in CKD
Impaired renal function -> less activation of vitamin D -> impaired mineralisation of bone
Stimulation of parathyroid glands caused by:
1) Decreased PO4 excretion, leading to increased plasma PO4
2) Decreased Ca2+ absorption, leading to decreased plasma Ca2+
Increased PTH & impaired mineralisation of bone -> increased bone resorption
Describe the pathophysiology of anaemia of chronic disease in CKD
Many factors contribute:
1) Decreased production of EPO from the pericytes
2) Blood loss
3) Absolute iron deficiency
4) Shortened RBC survival
Management: correct any underlying deficiencies, IV iron may be better tolerated than PO, aim for Hb 100-120
List complications of all long-term dialysis
CVS disease and sepsis
-peritonitis (from peritoneal dialysis) and staph aureus line infection (haemodialysis)
Amyloidosis – accumulation and polymerisation of B2-microglobulin
-molecule is normally excreted by the kidneys but is not removed by dialysis membranes -> deposition results in carpal tunnel syndrome & joint pains, particularly the shoulder
Renal bone disease