Renal Flashcards
Proximal tubule..
Main site for reabsorbtion
Aldosterone acts on..
Na channel in DCT to reabsorb water and sodium (secrete k and H)
Renal angiomyolipomas in what syndrome
TS
Peritonitis organisms in dialysis
SA 20% CONS 40% strep 20% pseudomonas 5%
Fanconi syndrome renal problem location
Proximal tubule dysfunction (RTA2), not reabsorbing all the good stuff so lose sodiuma nd don’t grow well and have tubular dysfunction so drink and wee lots
Causes: cystinosis and Lowes syndrome
In phaeo with HTN don’t use..
Bets blocker but use a blocker (phentolamine IV or oral phenoxybenzamine)
Persistently low C3 in…
Membranoprolif
RPGN presentation
Nephrotic or nephritic
Crescents on biopsy
Tx steroid
Presents with family history and haematuria
Alports genetic test and biopsy result?
Hereditary nephritis mainly XL (dominant)
Mutation in COL4 gene encoding type IV collagen which affects BM
Macroscopic haematuria
Biopsy variable thickness and splitting of BM - basket weave appearance
SNHL ears
Eyes cataracts, anterior lenticonus, macular abnormalities
ESRD 50% by 25
IgA nephropathy
Mostly boys Recurrent (at time of infection) Macroscopic haematuria Most are ok by 10% to EsRf Biopsy IgA deposits Tx steroids If bad
Three causes of nephrotic syndrome
Minimal change (steroids)
FSGN
Memb snouts nephropathy
Renal stone increased by high ? Diet
Na (decreases calcium absorption)
Present with FTT, recurrent episodes dehydration, hypercalciuria, 20% low serum mg, renal stones
Hypokalaemic metabolic acidosis
Bartter syndrome:
AR dysmorphic
Nephrocalcinosis
Like frusemide abuse
Present with hypokalaemic metabolic alkalosis, some mild growth failure, pr sent later, hypomagnesemia, hypocalciuria
Gitelman syndrome
AR defect na/cl CT
Like thiazide abuse
Prune belly =
Abdo wall defect, undescended testes, UT abnormalities
Granular casts in..
ATN
GFR gold standard
Inulin (gold standard but difficult to measure)
DTPA vs DMSA
Parenchyma defects
DMSA for structure/morphology - scarring, static scan, size and % function
DTPA for transit over time and looks for obstruction and drainage, how whole system is working, dynamic
Haematuria excretion rate increases with
Age and exercise
Proteinuria with fever, exercise, heart failure
Risk of nephritis in ahSP after 2m
2%
6 forms of steroid resistant nephrotic syndrome in childhood
Minimal change Membranoproliferative glomerulosis Membranous nephropathy Secondary (IgA, HSP, Lupus) FSGS Congenital
Syndrome causing childhood HTN
Liddle due to acting like there is high aldosterone (but it’s normal)
Best drug for reduction BP, proteinuria, preservation of renal function
ACEi
MCDK
1/4000, non heritable, unilateral nonfunctional cystic mass
Bilateral fatal often other kidney can make up for it but may have VUR - monitoring important
Campomelic dysplasia
SOX9, dysplasia, hydronephrosis
Agenesis kidney in what syndromes
Fraser
Kallman
Pallister-hall
Rubinstein-taybi
ADPKD
Mutation PKD
1/1000
Wide phenotype
Usually asymptomatic in childhood
ARPKD
Bilateral large echogenic kidneys
Mutation PKHD1
1/20000
With congenital hepatic fibrosis and hepatomegaly with portal HTN
Most frequent genetic cause CKD
Neohropnopthisis (tubuloingerstitial sclerosis - concentrating defect)
Causes of CKD
Hypoplasia/dysplasia
Nephronopthisis (normal kidney size)
Obstructive uropathy
Cystic
FSGN Chronic GN Alpert HUS Cortical necrosis
In chronic tubular defect - concentrating defect causes
Polyuria and polydipsia
Enuresis/nocturia
Electrolyte loss in urine
Causes of AKI
Sepsis HUS GN ATN Drugs Dehydration Interstitial nephritis Rhabdo Oncology Cardiac surgery Liver transplant
Tubular damage from what drugs
Aciclovir
Aminoglycosides
ATN urine results
Casts
Low osmolality
<40 urea/cr ratio
High Na
Two other causes HUS
Atypical in 10%
I.e.
Strep pneumoniae
Low C3
Anti GBM
May have pulmonary haemorrhage
Linear staining
Imaging small vs large echogenic kidney
Small structural
Large acute disease (ARF or GN)
Proteinuria
Sign of CKD and will progress - needs f/u
Orthostatic proteinuria
Normal in morning
Teens
Normalises
Nephrocalcinosis
Generalised echogenic appearance due to calcium deposits
- cortical nephrocalcinosis is often due to cortical necrosis – check renal function, BP etc
- Medullary and cortical – hypercalcaemia ( seen with excess Vit D) oxalosis (esp if calculi)
- Medullary alone – very long list of causes
Plasma osmolality
(2xplasma Na) + glu + urea
Chloride in urine
High in diuretic abuse, Bartters, Gitelmans
Low with vomiting and laxative abuse
Pneumococcal HUS pathophysiology
Neuraminidase uncovere T-cryptantigen which binds T IgM
Rituximab
Monoclonal antibody against CD20 causing rapid depletion of B cell populations
Mycophenolate mofetil mechanism of action and side effects
Inhibits T and B cell proliferation
GI, leukopenia, anaemia (not nephrotoxic)
Six causes of allograft dysfuncTION
DehydraTION MedicaTION InfecTION ObstrucTION RejecTION PrefusION problem
High tacrilomus level causes electrolyte low
MG
Tremour, alopecia
Cyclosporine SE
Hirsuitism and gingival hyperplasia
Post transplant lymohoproliferative disorder
Mononucleosis like lesions
Post transplant infection prophylaxis
CMV 3m valganciclovir
Cotrimox
Candida 1m nilstat (and with antibiotics)
Normal anion gap metabolic acidosis (not due to diarrhoea) causes
RTA
Type 1: unable to excrete H+ (urine mor alkaloid making a higher urine pH) low hCO3 level
Type 2: reduced bicarb reabsorption (assoc w Fanconi syndrome), acidic urine (no bicarb buffer)
Type 4: hyperkalaemia major feature, lose sodium in urine and keep potassium from mineralocorticoid def/insensitivity (hx obstructive uropathy or due to adrenal disease)
Type 3 RTA
Rare
Children have mental retardation, cerebral calcification and osteoporosis (carbonic anhydride deficiency)
Drug contraindicated in renal artery stenosis
ACEi
Renal artery stenosis assoc with what…
FiBromuscular dysplasia
Takayasu arteritis
NF1
Williams
Micrhaematuria resolves after how long with PSGN
2 years
Follow up renal after HSP for
3 months (risk 2% at 2m)
Minimal change presents with nephrotic syndrome and what feat on electromicroscopy
The three hallmarks of minimal change disease: diffuse loss of podocyte foot processes, vacuolation, and the appearance of microvilli.