Nephrology Flashcards
Autosomal Dominant Polycystic Kidney Disease (ADPKD) sonographic criteria (in individuals with family history of PCKD)
Age 15-39 - 3 or more cysts, unilateral or bilateral
Age 40-59 - 2 or more cysts in each kidney
Age 60 or older - 4 or more cysts in each kidney
Most common malignancy after renal transplant
Melanoma and non-melanomatous skin cancer Lymphoma Kidney Ureter / bladder Colorectal Lung
Absolute indications to commence dialysis
Uremic pericarditis or pleuritis
Uremic encephalopathy
Common indications to commence dialysis
Declining nutritional status (anorexia, weight loss, nausea)
Persistent or difficult to treat volume overload
Fatigue and malaise
Mild cognitive impairment
Refractory acidosis, hyperkalemia, hyperphosphataemia
Type 1 renal tubular acidosis (RTA) - investigations
Normal anion gap metabolic acidosis Urine pH more than 5.5 Urine anion gap positive Hypokalemia Hypercalcaemia Renal calculi
Type 1 renal tubular acidosis (RTA) - causes
Distal tubular defect with reduced H+ secretion.
- Autoimmune - SLE, Sjogrens, RA
- Drugs - amphotericin B, lithium, PPI, NSAID
- Chronic hepatitis
- Sickle cell anaemia
- Obstructive uropathy
- Thyroid disorders
Type 2 renal tubular acidosis (RTA) - investigations
Normal anion gap metabolic acidosis (milder than type 1)
Urine pH more than 5.5 - if treated with alkali therapy
Urine pH less than 5.3 - if untreated
Type 2 renal tubular acidosis (RTA) - causes
Proximal tubular defect with failure to reabsorb HCO3.
- Fanconi’s syndrome
- Multiple myeloma
- Amyloidosis
- Interstitial nephritis
- Heavy metal poisoning
- Antivirals - tenofovir
Type 3 renal tubular acidosis (RTA) - causes
Mixed features of both distal and proximal RTA.
- Inherited carbonic anhydrase (CA) II deficiency - rare autosomal recessive disorder
Type 4 renal tubular acidosis (RTA) - investigations
Normal anion gap metabolic acidosis
Urine pH less than 5.5
Urine anion gap positive
Hyperkalemia
Type 4 renal tubular acidosis (RTA) - causes
Aldosterone deficiency or distal tubule resistance to aldosterone.
- Diabetic nephropathy
- Drugs - NSAID, ACEi, ARB, spironolactone, tacrolimus
Mechanism of renal failure in gentamicin toxicity
Acute tubular necrosis
Mechanism of renal failure in multiple myeloma
Cast nephropathy (41%) Amyloidosis (30%) Monoclonal Ig deposition disease (19%) Interstitial nephritis (10%)
Mechanism of action - frusemide
Location - Thick ascending limb of loop of Henle
Channel - Na-K-2Cl carrier on tubular lumen
Action - competes for Cl site, reduces reabsorption (including Mg)
Mechanism of action - hydrochlorothiazide
Location - distal tubule connecting segment
Channel - Na-Cl cotransporter
Action - compete for Cl site, reduce reabsorption, (increases Ca reabsorption)
Mechanism of action - spironolactone
Location - cortical collecting tubule
Channel - aldosterone sensitive Na channel
Action - compete and inhibit mineralcorticoid receptor
Mechanism of action - acetazolamide
Location - proximal tubule
Action - inhibits carbonic anhydrase, reduces HCO3, Na, Cl reabsorption
Mechanism of renal bone disease
- Increased phosphate - due to low PO4 filtrate load
- Secondary hyperparathyroidism
- Decreased calcium
- Decreased calcitriol (1,25 dihydroxy vitamin D)
Mechanism of minimal change disease
- Podocyte injury
- Immune mediated
Mechanism of membranous glomerulonephritis
- Anti PLA2-R (phospholipase A2 receptor antibodies) on podocytes
Mechanism of membranoproliferative glomerulonephritis
- Immune complex OR complement mediated (less common)
- Proliferation of glomerular cells
- Systemic inflammatory cell influx
Mechanism of focal sclerosing glomerulonephritis
- Similar to minimal change
- Podocyte injury due to circulating factors
Mechanism of IgA nephropathy
- Mesangial deposition of IgA
- Mesangial cell proliferation
- Complement activation
Liddle’s syndrome
- Abnormality in ENaC channel (acted on by spironolactone)
- Collecting duct
- Hypokalemia
- Hypertension
- Metabolic alkalosis
