Renal Flashcards
3 endocrine roles of the kidney
Renin (vasoconstriction as part of RAAS)
EPO
vit D metabolism
What stimulates EPO?
hypoxia
anaemia
renal ischaemia
When is EPO increased?
PKD and RCC
causes polycythaemia
When is EPO decreased?
CKD
causes normocytic normochromic anaemia
Describe metabolism of vit D
natural vit D (cholecalciferol) –> goes to liver, becomes 25(OH)D3 —> in proximal tubule, under 1a hydroxylase becomes 1,25 (OH)2 D3
What is vit D needed for?
bone mineralisation
absorption of calcium and phosphate from gut
What regulates the formation of 1,25 (OH)2 D3?
PTH, phosphate and negative feedback
What causes agenesis of the kidney?
collecting duct (from ureteric buds) fails to fuse with nephrons (from metanephric mesoderm) can be unilateral (or bilateral - Potter's syndrome -> death)
remaining kidney hypertrophies, may have abnormalities (hydronephrosis, malrotation)
renal function may be normal
often associated with other congenital abnormalities
What are common problems with congenital kidney issues, eg hypoplasia, horse-shoe kidney?
Often issues with malrotation and prone to reflux, obstruction, infection and stones
What are the 3 general causes of glomerulonephritis?
Hereditary (Alport’s, Fabry’s)
Primary
Secondary (SLE, DM)
5 levels of severity of glomerular disease
- asymptomatic haematuria/ proteinuria
- nephrotic syndrome
- nephritic syndrome
- rapidly progressive glomerulonephritis
- CKD
Clinical features of nephrotic syndrome
Proteinuria, hypoalbuminaemia, oedema, hyperlipidaemia (hepatic lipoprotein secondary to protein losses)
Clinical features of nephritic syndrome
Oliguria/ anuria, HTN, fluid retention, haematuria, uraemia, some proteinuria
Clinical features of rapidly-progressive glomerulonephritis?
Haematuria, oliguria, hypertension –> renal failure
Examples of primary glomerulonephritis typically giving nephrotic syndrome
Minimal change disease
Membranous glomerulonephropathy
Focal segmental glomerulosclerosis
Who usually gets minimal change disease?
typically kids under 6
seen on electron microscopy
cause unknown, maybe circulating immune-complexes
good prognosis in kids, variable in adults
Most common cause of nephrotic syndrome in adults?
Membranous glomerulonephropathy
chronic - causes 40% nephrotic
What is membranous glomerulonephropathy?
widespread glomerular basement thickening caused by Ig deposition - causes hyalinisation and death of individual nephrons
Causes of membranous glomerulonephropathy
85% are idiopathic
secondary causes: infections (hep B, malaria, syphilis) tumours (melanoma, Ca bronchus, lymphoma) drugs systemic (SLE)
Prognosis depends on cause - 1/3 get CKD
Examples of primary glomerulonephritis typically giving nephritic syndrome
Berger’s disease (IgA nephropathy)
Rapidly progressive glomerulonephritis
Focal proliferative glomerulonephritis
Most common cause of primary glomerulonephritis?
Berger’s
no effective treatment - 20% > CKD
What causes Berger’s disease?
IgA nephropathy
usually affects young men after an URTI
What are the causes of secondary glomerulonephritis?
Post-streptococcal GN Non-strep GN SLE Henoch-Schonlein purpura Bacterial endocarditis Diabetic glomerulosclerosis Amyloidosis Goodpasture's syndrome Microscopic polyarteritis nodosa Wegener's granulomatosis
When does post-strep GN occur?
1-3 weeks after group A beta-haemolytic strep infection (tonsils, pharynx, skin)
How is post-strep GN treated?
Conservative/ abx for remaining infection
Kids recover well but 40% adults develop HTN/ renal impairment
What % SLE have kidney involvement?
75% - often most significant of lesions
caused by immune-complex deposition
What causes HSP?
can follow URTI - immune-mediated systemic vasculitis
Which organs does HSP affect?
Skin (purpuric rash over legs, arms, arse)
Joints (pain)
Intestine (abdo pain, vomiting, bleeding)
Kidney (third develop lesions identical to IgA nephropathy)
How does bacterial endocarditis cause glomerulonephritis?
Emboli
Immune-complex deposition
Presents with haematuria and fluid retention
Why can Alport’s not get Goodpasture’s?
Lack the Goodpasture’s antigen - abnormality of BM collagen IV
Clinical features of Alport’s syndrome
ocular abnormalities - sensorineural deafness - renal failure
X-linked
(female carriers may have microscopic haematuria)
Clinical features of Fabry’s syndrome
X-linked
metabolic defects due to missing enzyme
deposits accumulate in kidney, skin, vascular system (associated with angina + HF)
most die in 50s