Kidney Flashcards
What are the indications for starting dialysis? (4)
- Hyperkalaemia
- Uraemia
- Metabolic acidosis
- Pulmonary oedema
When do you start dialysis in an anuric patient?
Only when they have indications
What complications can uraemia cause? (2)
- Encephalopathy
- Pericarditis
What is the pathophysiology of rhabdomyolysis?
Breakdown of muscle → release of CK
What is the key investigation in rhabdomyolysis?
CK
What is unique about the dipstick result in rhabdomyolysis?
+ve for blood but when observed under microscope there will be no RBCs - myoglobin
Why is rhabdomyolysis dangerous for the kidneys?
Risk of ARF as myoglobin is nephrotoxic
What is the management of rhabdomyolysis?
0.9% saline
What is the best measure of kidney function and what’s the normal value?
GFR = best measure of kidney (normal = 120ml/min)
How do we estimate GFR?
Using clearance - volume of plasma cleared of a marker substance per unit time
What is the formula for clearance?
Clearance = (urinary concentration of marker x volume) / plasma concentration of the marker
What are the 3 criteria for using a marker to estimate GFR? (3)
- Freely filtered
- Not bound to plasma proteins
- Not reabsorbed / secreted by tubules
What is the gold-standard marker of GFR and why isn’t it used clinically?
- Inulin is the gold-standard marker
- Not used in clinical practice - requires an IV steady-state infusion
What are the characteristics of blood urea as a marker? (4)
- Endogenous marker (by-product of protein metabolism)
- Freely-filtered by variable reabsorption by tubular cells
- Dependent on nutrition, GI bleeding, hepatic function
- Not used as a marker of GFR but of dehydration
What are the key points about serum creatinine? (3)
- Derived from muscle cells
- Freely filtered, active secretion into tubules
- CKD-EPI equation uses creatinine clearance to calculate eGFR - this is what we use in clinical practice
What are the characteristics of Cystatin C? (3)
- Alternative endogenous marker to creatinine - generated by nucleated cells
- Freely filtered, but almost completely reabsorbed
- Not really used clinically
What is the gold standard for measuring proteinuria?
spot urine protein:creatinine ratio
Is 24-hour urine collection commonly used for measuring proteinuria?
no
What is the gold standard imaging for kidney stones?
CTKUB (CT Kidneys, Ureters, Bladder)
What is the basic definition of AKI?
Reduction in GFR over 1 week - reversible
What are the three main categories of AKI? (3)
- Pre-renal
- Renal
- Post-renal
What is the main mechanism of pre-renal AKI?
Reduced renal perfusion
What are the causes of pre-renal AKI? (7)
- Shock
- Renal artery stenosis
- Haemorrhage
- Hypotension
- Calcineurin inhibitors
- NSAIDs/ACIs/ARBs
- Diuretics
What are the two key adaptive mechanisms that maintain renal perfusion? (2)
- Myogenic stretch - afferent arteriole if stretched constricts to reduce high pressure to the bowman’s capsule
- Tubuloglomerular feedback - high Cl- in the distal tubule → constriction of afferent arteriole
What are the key characteristics of pre-renal AKI? (3)
- NO structural renal damage
- Responds immediately to restoration of circulating volume
- Often precipitated by starting an ACEi
What is pre-renal AKI often precipitated by?
ACEi
What is the key characteristic of renal AKI?
Structural renal damage is present
What are the causes of renal AKI? (8) (MAGIC VAD)
- M - Multiple Myeloma & Myoglobin
- A - Amyloidosis & ATN
- G - Glomerulonephritis
- I - Interstitial disease
- C - Contrast
- V - Vasculitis
- A - Aminoglycosides, Amphotericin, Aciclovir
- D - Drugs (other nephrotoxic)
What is the most common cause of ATN?
Most commonly caused by prolonged pre-renal AKI → ischaemic injury
What are the obstructive causes of post-renal AKI? (4)
- Renal stone
- BPH
- Transitional cell carcinoma
- Extrinsic mass pressing on ureter
What happens if post-renal AKI is managed quickly vs slowly? (2)
- If managed quickly - restore GFR with no structural damage
- If managed slowly - glomerular ischaemia & tubular damage
What are the causes of CKD? (6)
- DM (most common)
- Hypertension
- Atherosclerosis
- Chronic glomerulonephritis
- Prostate disease
- PCKD
Most common cause of CKD?
Diabetes
What are the metabolic consequences of CKD? (4)
- Metabolic acidosis
- Hyperkalaemia
- Normochromic anaemia
- Secondary/tertiary hyperparathyroidism
What are the major complications of CKD? (4)
- Uraemia (leading to cardiomyopathy, encephalopathy)
- Renal osteodystrophy
- CVD (most likely to kill them, highly calcified plaques)
- Bone disease
What are the three types of bone disease in CKD? (3)
- Osteitis fibrosa cystica → bone cysts, Brown’s tumours
- Adynamic bone disease - resistance to PTH in bones → low bone turnover
- Osteomalacia - inadequate mineralisation of bone
What are the 6 key aspects that need management in CKD? (6)
Remember “AH HMVP” (Ah, Help My Vitamin P!)
- A - Anaemia
- H - Hyperkalaemia
- H -Hyperparathyroidism
- M - Metabolic acidosis
- V - Vitamin D deficiency
- P - Phosphate (Hyperphosphataemia)
How is metabolic acidosis managed in CKD?
Oral sodium bicarbonate
What is the management for hyperkalaemia in CKD?
Dietary management
How is anaemia managed in CKD?
Artificial EPO (Erythropoietin)
What are the two approaches to managing hyperphosphataemia in CKD? (2)
- Dietary management
- Phosphate binders
How is Vitamin D deficiency managed in CKD?
1-alpha calcidol
How is hyperparathyroidism managed in CKD?
Cinacalcet - increases sensitivity of calcium sensing receptors → decreased PTH
