Renal Flashcards
Reoccurrence of renal disease following renal transplant
Fastest - FSGS
Won’t reoccur - Alport’s disease
Primary action of vasopressin?
Acts on renal collecting ducts via V2 receptors to increase water permeability (cAMP-dependent mechanism) which leads to decreased urine formation
Mechanisms regulating release of vasopressin
Hypovolemia decreases firing of arterial stretch receptors = increased ADH
Hypotension decreases arterial baroreceptor firing = enhanced sympathetic activity = increased AVP release
Hypothalamic osmoreceptors stimulate ADH release when osmolarity rises
Angiotensin II receptors in the hypothalamus - increased angiotensin II = ADH release
Features of Fanconi Syndrome
Type 2 (proximal) renal tubular acidosis Polyuria Aminoaciduria Glycosuria Phosphaturia Osteomalacia
Nephrotic Syndrome
= proteinuria, oedema, hypoalbuminemia Minimal change Membranous GN FSGS Amyloidosis Diabetic Nephropathy
Nephritic Syndrome
= haematuria, hypertension
IgA nephropathy
Rapidly progressive GN
Alport
Rapidly progressive GN
ANCA associated vasculitis (most common) - pauci immune, necrosis and eosinophils
Anti GBM disease - linear IgG on IF
SLE - mixed, complement and antibodies
ANCA associated vasculitis
Granulomatosis with Polyangitis - granulomatous - cANCA - cytoplasms PR3 = worse prognosis Microscopic Polyangitis - no granulomas - pANCA - perinuclear - MPO Eosinophilic Granulomatosis with Polyangitis - asthma, eosinophilia, granulomas - either PR3 or MPO
Alport’s Syndrome is due to a defect in
Type IV collagen
AL (primary) Amyloidosis
Most common form
L for immunoglobulin Light chain fragment
Due to myeloma, Waldenstrom’s, MGUS
Features: nephrotic syndrome, cardiac and neuro involvement, hepatosplenomegaly, macroglossia
AA (secondary) amyloid
A for precursor serum amyloid A protein, an acute phase reactant
Seen in chronic infection / inflammation
E.g. TB, RA, bronchiectasis, Crohn’s, ank spond, psoriatic arthritis
Features: renal involvement - often leads to ESRF
Beta-2 microglobulin amylodosis
Precursor protein is beta-2 microglobulin = major part of HLA complex
A/w patients on dialysis
Extra renal manifestations of ADPKD
Liver cysts
Berry aneurysms
Cardiovascular: mitral valve prolapse, mitral / tricuspid incompetence, aortic root dilatation, aortic dissection
Cysts in other organs: pancreas, spleen
Genetic mutations in ADPKD
Chromosome 16 (PKD 1) = non clonal expansion of tubular epithelial cell types; polycystin 1 (mechanosensor)
Chromosome 4 (PKD 2) Polycystin 2 (calcium channel ion)
Tuberous sclerosis
Autosomal dominant
Mutations in TSC1 or TSC2 gene
Major criteria: facial angiofibromas, >3 hypomelanotic macules, kidney angiomyolipomas, retinal hamartomas
Minor criteria: nonrenal hamartomas, multiple kidney cysts, dental abnormalities
Main site of potassium reabsorption in the kidney?
Proximal convoluted tubule
As GFR declines, urinary creatinine clearance overestimates GFR because Cr is
Secreted by the tubules
Drugs that can be cleared by haemodialysis
BLAST Barbituate Lithium Alcohol (methanol, ethylene glycol) Salicylates Theophylline
Main site of sodium reabsorption in the nephron?
Proximal convoluted tubule
Site of action for frusemide?
Thick ascending loop of Henle
Blocks Na-Cl cotransporter (NKCC2)
Site of action for thiazides / indapemide?
Distal convoluted tubule
Site of action for Spironolactone?
Collecting duct
Lithium absorption
Reabsorbed in the proximal tubule
Lithium absorption follows sodium uptake
Therefore increased risk of toxicity with diuretics and hypovolemia
Order of events in the renin-angiotensin system?
- Kidneys sense low BP
- Release renin into the blood
- Renin causes production of Angiotensin I
- ACE converts angiotensin I to angiotensin II
- Angiotensin II stimulates the release of aldosterone, ADH and thirst
- Water follows sodium
- Blood volume goes up = BP goes up
Which cell in the kidney makes erythropoietin?
Peritubular cell
Urinary pattern of glomerular disease or vasculitis?
haematuria with red cell casts, dysmorphic red cells, heavy proteinuria or lipiduria
Urinary pattern of acute tubular necrosis in renal failure?
Multiple granular and epithelial cell casts with free epithelial cells
Secondary causes of membranous nephropathy
SLE Drugs - NSAIDs, penicillamine, gold Hepatitis B and C Malignancy- solid organ Timor’s HSCT Kidney transplant Syphilis
Distal (Type 1) Renal Tubular Acidosis
Impaired secretion of hydrogen ions = urine pH >6.0, kidney potassium wasting, hypokalemia
Usually secondary to autoimmune disease (Sjogrens most common, SLE, RA)
Proximal (type 2) Renal tubular acidosis
Caused by reduction in bicarbonate reabsorption in the proximal tubule
Causes urine pH<5.5
Causes Fanconi Syndrome
Diagnosis of ADPKD
2 or more cysts in one kidney and at least one cyst in the contralateral kidney - young pt (by 30yo)
4 or more cysts in each kidney for patient more than 60yo
Gitelman’s syndrome
Defect in distal tubule = thiazides
Normotensive, metabolic alkalosis, hypokalemia, hypomagnesemia, hypocalciuria
Bartter’s Syndrome
Autosomal recessive
Severe hypokalemia due to defective chloride secretion at the NKCC2 cotransporter in the ascending loop of henle (frusemide)
Polyuria, polydipsia, hypokalemia, normotension, weakness
Liddell Syndrome
Increased number Na channel in collecting duct which results in increased Na reabsorption and potassium excretion
Fibromuscular dysplasia
Female
Age 15-40
Severe HTN with evidence of target organ damage
Mild hypokaklemic metabolic alkalosis and high renin suggest underlying renovascular hypertension
Abdominal bruit
Diagnosis: intracellular-arterial digital subtraction angiography - string of beads appearance
Most common histology can feature in chronic allograft nephropathy?
Chronic interstitial nephritis
Dent Disease
X-linked recessive disorder of the proximal tubules
Proteinuria, hypercalciuria, nephrocalcinosis, kidney stones, renal failure, Ricketts
Due to mutation in CLCN5 gene
Familial renal glycosuria
Mutations in the SLC5A2 gene coding for SGLT2 in the proximal tubule
Urine glucose excretion but normal BSL
Actions of Atrial Natriuretic Peptide (ANP)
Causes marked natriuresis
Lowers BP
Inhibits secretion of renin and vasopressin
Decreases responsiveness of the kidney to stimuli that would normally increase aldosterone secretion
Increased ANP is a/w increased extra cellular fluid volume
