Renal Flashcards
Adrenal cortex mnemonic?
GFR-ACD
- Zona Glomerulosa (outside) - mineralocorticoids (mainly Aldosterone)
- Zona Fasciculata (middle): glucocorticoids, mainly Cortisol
- Zona Reticularis (on inside): androgens, mainly Dehydroepiandrosterone (DHEA)
Summary of RAAS?
-
Renin
- Released by JGA cells in kidney in response to reduced renal perfusion, low sodium
- Hydrolyses angiotensin to form angiotensin I
- Stimulated by - low BP/low renal perfusion, hyponatraemia, sympathetic nerve stimulation, catecholamines, erect posture
- Reduced by - B-blockers, NSAIDs
-
Angiotensin
- ACE (lung) converts angiotensin I to angiotensin II
- Vasoconstriction –> increased BP
- Stimulates thirst and stimulates aldosterone/ADH release
-
Aldosterone
- Released by zona glomerulosa in response to raised angiotensin II, K+ and ACTH levels
- Causes retention of Na+ in exchange for K+/H+ in distal tubule
Urinalysis patterns?
Calcium metabolism?
Renal bone disease summary? And clinical manifestations?
- Osteitis fibrosa cystica
- AKA hyperparathyroid bone disease
- Adynamic
- Reduction in cellular activity (both osteoblasts and osteoclasts) in bone
- May be due to over treatment with vitamin D
- Osteomalacia
- Due to low vitamin D
- Osteosclerosis
- Osteoporosis
Management of Renal Anaemia?
- Correction of iron with IV if needed
- Ferritin should be > 200 ng/mL before starting EPO
- EPO is used to target Hb 10-12 (>11 or hematocrit >33%) reach the target within 4 months
- Corrected Hb of > 13.5 is associated with HTN crisis
- Hb < 10.5 increased risk of seizures.
Side effects of EPO?
- HTN and HTN crisis, potentially encephalopathy and seizures (BP increased in 25% of patients)
- EPO induced seizures occurs after 90 days fro starting the treatment
- Bone aches
- Flu-like symptoms
- Skin rashes, urticaria
- Pure red cell aplasia* (due to antibodies against erythropoietin)
- Raised packed cell volume (PCV) = HCT –> increased risk of thrombosis (e.g. Fistula)
- Iron deficiency 2nd to increased erythropoiesis
Reasons why people fail to respond to EPO?
- Iron deficiency
- Inadequate dose
- Concurrent infection/inflammation
- Hyperparathyroid bone disease
- Aluminum toxicity
What mediates hyperacute graft rejection?
IgG
Graft survival stats?
Cadaveric
- 1 year = 90%
- 10 years = 60%
Living donor
- 1 year = 95%
- 10 years = 70%
Post-op problems for renal transplant?
Up to 4 months post-op (can cause graft dysfunction)
- Acute rejection: risk is great in 1st 2 weeks occurs in 30-50% of cases
- Ciclosporin toxicity
- ATN of graft
- Vascular thrombosis
- Urine leakage
- UTI
Management of acute (<6 months) graft failure?
Causes of chronic graft failure (>6 months)?
Acute
- Steroids
- If resistant use monoclonal antibodies
Chronic
- Chronic allograft nephrotherapy
- Ureteric obstruction
- Recurrence of original renal disease
Autosomal dominant polycystic kidney disease - types, diagnostic criteria?
Types
Loci = PKD1 and PKD2 - code for polycystin-1 and 2 respectively
Investigation/Criteria
Abdominal ultrasound
- Recommended after 20 years of age (risk of false -ve)
- <30 yrs - 2 cysts, unilateral or bilateral
- 30-59 yrs - 2 cysts in both kidneys
- >60 yrs - 4 cysts in both kidneys
Management
- Analgeisa
- Abx for UTIs
- HTN control
- Transplantation for ESRF
Conditions associated with ADPKD?
- Colonic diverticula
- Mitral valve prolapse
Autosomal recessive PKD?
- Much less common than ADPKD
- Chromosome 6
- Dx - usually on prenatal USS or early infancy with abdo masses and renal failure
- ESRF in childhood
- Liver involvement
Nephrotic syndrome causes?
-
Glomerulonephritis (80%)
- Minimal change GN (75% children)
- Membranous GN
- Focal segemnental glomerulosclerosis
-
Systemic disease
- Amyloid
- SLE
-
Drugs
- Gold (sodium aurththiomalate), penicillamine
-
Others
- Congenital
- Neoplasia - carcinoma, lymphoma, leukaemia, myeloma
- Infection - bacterial endocarditis, hep B, malaria
- Renal vein thrombosis
Complications of nephrotic syndrome
- Infection due to urinary immunoglobulin loss
- Thromboembolism related to loss of antithrombin III and plasminogen in the urine
- Hyperlipidemia
- Hypocalcemia (vitamin D and binding protein lost in urine)
- Acute renal failure could be due to thrombotic renal veins - loin pain and haematuria.
Types of glomerulonephritis?
-
Membranous GN (Commonest type)
- Proteinuria/nephrotic syndrome/CRF
- Cause - infections, rheumatoid drugs, malignancy, SLE
- Biopsy - sub-epithelial immune complex deposition (IgG, C3)
- 1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop CRF
-
IgA Nephropathy (Commonest worlwide cause of GN)
- Young adult with painless haematuria after UTI
- Associated with HSP, coeliac, dermatitis herpetiformis
- Mesangial hypercellularity, +ve immunofluoresence for IgA and C3
- Good prognosis - frank haematuria
- Poor prognosis - male, proteinuria, HTN, smoking, high lipids
-
Diffuse Proliferative GN
- Post-streptococcal glomerulonephritis in a child
- Nephritic syndrome/ARF
- Most common form of renal disease in SLE
-
Minimal Change Disease
- Child with nephrotic syndrome
- Causes - Hodgkin’s, NSAIDs
- Good response to steroids, next line cyclophosphamide
- Biopsy - podocyte fusion
- Rule of 1/3
-
Focal Segmental GN
- Idiopathic, or 2ndry to HIV/Heroin, Alport’s, Sickle cell
- Proteinuria/nephrotic syndrome/CRF
-
Rapidly Progressive GN (Crescenteric GN)
- Rapid onset –> ARF
- Causes - Goodpasture’s, ANCA +ve vasculitis (Wegener’s)
-
Mesangiocapillary GN (Membranoproliferative)
- Nephrotic syndrome, haematuria, proteinuria
- Poor prognosis
- Type 1 - cryoglobulinaemia, hepatitis C –> low C4
- Type 2 - partial lipodystrophy –> low C3