Nephrology Flashcards
Acute Interstitial Nephritis
Causes 25% of drug induced AKI.
Causes - penicillin, rifampicin, NSAIDs, allopurinol, furosemide, SLE, sarcoid, Hanta virus, staph
= fever, rash, arthralgia, renal impairment, HTN
Inv - eosinophilia, sterile pyuria, WC casts
TIN with Uveitis
= young females, fever, weight loss, painful red eyes
Inv - leukocytes and protein
Acute Tubular Necrosis
Most common cause of AKI, reversable in early stages
Causes
Ischaemic - shock, sepsis
Nephrotoxins - aminoglycosidess, myoglobin (rhabdomyolisis), radiocontrast, lead
= oligouric phase, polyuric, recovery
Inv. - urea, creatinine, K, muddy brown casts
Acute Tubular Necrosis vs Pre-renal Uraemia
-Poor reabsorption of Na and water in ATN but low osmolarity as a lot more water relative to Na
-In pre-renal uraemia, the kidneys hold on to Na to preserve volume
Urine sodium - pre-renal (v), ATN (^)
Urine osmolarity - pre-renal (^), ATN (v)
Fluid challenge - pre-renal (good), ATN (poor)
Urea:creat - pre-renal (^), ATN (normal)
ADPKD
Type 1 - 85%, Chr 16, earlier renal failure
Type 2 - 15%, Chr 4
= HTN, recurrent UTI, abdo pain, renal stones, haematuria, CKD, liver cysts, berry aneurysms
Screening using abdo US = two cysts <30yrs, two cysts bilaterally <60yrs, four cysts bilaterally 60+
-> Tolvaptan (vasopressin 2 antagonist, slows progression)
Slightly increased risk of RCC
ARPKD
Less common, Chr 6 (fibrocystin)
= (infancy) abdo mass, renal failure, Potter’s syndrome 2nd to oligohydramnios, liver fibrosis
Diagnosed on prenatal US, biopsy (lesions at right angle to cortical surface)
Alport’s
X linked dominant, more severe in males
Defect in T4 collagen = abnormal GBM
= (childhood) microscopic haematuria, renal failure, bilateral SN deaf, lenticonus (lens protudes into ant. chamber), retinitinis pigmentosa
Inv - biopsy (splitting of lamina densa, basket weave), genetic testing
Amyloidosis
Extracellular deposition of amyloid
Inv. - congo red staining gives apple green birefringence, serum amyloid precursor scan, biopsy (skin, rectum, abdo)
Goodpasture’s (anti-GBM)
Anti-GBM Ab against T4 collagen, small vessel vasculitis
RF - 2M:F, peak in 20s and 60s
= pulmonary haemorrhage, rapidly progressive GN (protein and blood)
Inv - biopsy (IgG deposits along GBM), raised transfer factor
-> plasma exchange, steroids, cyclophosphamide
AV Fistula
Direct connection between artery and vein, 6-8wks to develop
Preferred access for haemodialysis
Comp - infection, thrombosis, stenosis, steal syndrome
Diabetetes Insipidus
Cranial (v ADH secretion by pit)
Causes - idio, head injury, pit surgery, sarcoid, haemochromatosis, craniopharyngioma, DIDMOAD
Nephrogenic (insensitivity to ADH)
Causes - lithium, ^Ca, v K, genetic (aquaporin)
= polyuria, polydipsia, high plasma osmolarity vs low urine osmolarity, water deprivation test
-> desmopressin for cranial, thiazides and low salt for nephro
EPO
Hematopoietic growth factor, for production of RBCs
Used in CKD, chemotherapy
SE: accelerated HTN (encephalopathy, seizures), bone aches, flu-like, rash, pure red cell aplasia (Ab against EPO), thrombosis (^PCV), iron def
If not responding to EPO, think iron def
Renal Artery Stenosis
2nd to atherosclerosis, 10% fibromuscular dysplasia (^^F)
Link - takayasus arteritis
= HTN, flash pulmonary oedema, AKI after ACEi
Focal Segmental Glomerulosclerosis
Nephrotic, young adults
Causes - idio, HIV, heroin, Alport’s, sickle cell, 2nd to IgA nephropathy
Inv - biopsy (FS sclerosis, effacement of feet)
-> steroids +/- IS
*high recurrence after renal transplant
Haemolytic Uraemic Syndrome
Thrombosis in small blood vessels leads to thrombocytopenia and haemolysis
Causes - Shiga toxin-producing E.coli 0157, pneumococcal, HIV
= kids, AKI, microangiopathic hemolytic anemia and thrombocytopenia
Inv - FBC, U&Es, blood film (schistocytes, helmet cells), negative coombs, stool culture
-> supportive (fluids, blood, dialysis)
NO Abx
HSP
IgA mediated small vessel vasculitis, self-limiting, overlaps with IgA nephropathy
= child post-infection, palpable purpuric rash, over bum/ extensors, local swelling, abdo pain, polyarthritis
Inv - monitor BP and urinalysis
-> analgesia, supportive
IgA Nephropathy
Bergers disease
Commonest cause of GN in world
= young man, macroscopic blood 1-2d after URTI, no proteinuria
-> ACEi if persistent proteinuria
Membranoproliferative GN
Also called mesangiocapillary
Type 1 - 90%, linked to Hep C, biopsy (immune deposits, tram-track)
Type 2 - dense deposit disease, low C3, C3b nephritic factor, biopsy (dense deposits)
Type 3 - linked to hep B and C
-> steroids
Membranous GN
Commonest GN in adults, 3rd most common cause of ESRF
Causes - idio (APL Ab), cancer (prostate, lung, lymph), penicillamine, NSAIDs, AI, hep B, malaria, syphilis
Inv - biopsy (spike and dome EM)
-> all get ACEi/ ARB, if severe give steroids + cyclophosphamide
1/3 spont remit, 1/3 remain proteinuric, 1/3 ESRF
Minimal Change Disease
Most common GN in kids (75%)
Causes - ^^idio, NSAIDs, rifampicin, Hodgkin’s, thymoma, glandular fever
= nephrotic, normal BP, selective proteinuria (mid-size, albumin/ transferrin)
Inv - normal LM, fusion of podocytes/ foot effacement EM
-> PO steroids
1/3 have one episode, 1/3 infrequently relapse, 1/3 frequent
Nephrotic Syndrome
Proteinuria - >3g / 24hr
Low albumin - <30
Oedema
- Loss of AT-3 and protein C = thrombosis
- Loss of thryoxine binding globulin = v total but not free thyroxine levels
- ^hepatic lipogenesis due to falling oncotic pressure = high cholesterol
Contrast Nephrotoxicity
25% inc in creatinine within 2-5d of contrast
RF - known renal issues, >70yrs, dehydration, HF, NSAIDs
Prevention - IV 0.9% NaCl at 1ml/kg/hr for 12 hours before and after
If at high risk, stop metformin for 48hrs before and until renal function is normal
Post Strep GN
7-14 days after group A hemolytic strep - pyogenes
Immune complex deposition in glomerulus causing acute diffuse proliferative GN
= young children, headache, malaise, haematuria, oedema (proteinuria), oliguria, HTN
Inv - v C3, ^ASO, biopsy (subepithelial humps EM, granular/ starry sky IF)
Rapidly progressive GN
Rapid loss of renal function associated with epithelial crescents in glomeruli
Causes - Goodpasture’s, Wegener’s, SLE, microscopic polyarteritis
= nephritic syndrome (blood, protein, oliguria, HTN)
Renal papillary necrosis
Causes -
Severe acute pyelo
Diabetic nephropathy
Obstructive nephropathy
Analgesic nephropathy (NSAIDs)
Sickle cell anaemia
= macro haematuria, loin pain, proteinuria
Graft rejection
HLA system is the major histocompatibility complex in humans, Chr 6
Most important HLA is DR then B then A
Post-op complications - ATN of graft, vascular thrombosis, urine leak, UTI
Hyperacute (min-hrs)
Pre-existing Ab against ABO or HLA, T2HS, widespread thrombosis
-> Need to remove
Acute (<6months)
HLA mismatch, cell-mediated
= no symptoms, ^creat, pyuria, proteinuria
-> steroid/ IS
Chronic (>6m)
Ab and cell-mediated, fibrosis
Post-transplant IS- monitor BP, glucose, lipids, renal function, risk of SCC and BCC
Rhabdomyolysis
Skeletal muscle breaks down, releases breakdown products into blood (myoglobin, potassium, phosphate and CK)
RF - fall, seizure, marathon runner, statins (w/ clarithro), crush
= AKI (^^creat), 5x normal CK, myoglobinuria (dark, dip +blood), v Ca (binds myoglobin), ^K, ^phosphate, met acidosis
-> IV fluids, urinary alkalinization
Dipstick +blood
Transient
UTI, period, vig. exercise, sex
Persistent
Cancer, stones, BPH, prostatitis, urethritis (chlamydia), kidney problems
Red but not +blood = beetroot, rifampicin, doxorubicin
Stauffer Syndrome
Paraneoplastic disorder, 5% of RCC
? ^IL6-> hepatic dysfunction (cholestasis, hepatosplenomegaly)
= sudden RUQ pain, nausea, jaundice and deranged LFTs
Drugs to Stop in AKI
Diuretics
ACEi/ ARB
Metformin (risk of toxicity)
NSAIDs - keep aspirin 75mg
Lithium (risk of toxicity)
Aminoglycosides
Digoxin (rick of toxicity)
RRT Indications
A - Acidosis
E - Electrolytes (^K)
I - Intoxicants (lithium, salicylate)
O - Overload
U - Uraemia (pericarditis, encephalopathy)
Renal Tubular Acidosis
^Cl metabolic acidosis due to renal tubular pathology (normal anion gap)
Type 1
Causes - RA, SLE, Sjogren’s, NSAIDs
Distal tubule unable to excrete H+, loss of K
= hyperventilation, FTT, renal stones
-> treat with bicarbonate
Type 2
Causes - Fanconisyndrome, Wilson, acetazolamide
Prox tubule can’t reabosorb bicarb, loss of K
= osteomalacia
Type 3
Mixed, extremely rare
Type 4 (most common)
Causes - hypoaldosteronism, DM
Reduced proximal ammonium excretion, ^K
-> fludrocortisone and bicarbonate
Causes of AKI
Prerenal (most common)
Inadequate blood supply to kidneys
- hypovolemia, renal artery stenosis
Renal
Intrinsic damage (only one with proteinuria)
- GN, AIN, ATN, rhabdomyolysis, tumour lysis
- gentamicin if prev. treatment for UTI
Post-renal
Back pressure reduces function of the kidney
- renal/ ureteric stone, BPH, external compression of ureter
Common causes of CKD
DM
HTN
Age
PCKD
Meds - NSAIDs, PPI
Glomerulonephritis
Chronic pyelonephritis
Anaemia of CKD
Causes - v EPO production, v iron absorption
Normocytic normochromic anaemia, usually when GFR<35
-> check iron status, EPO
Renal Bone Disease
In CKD there is;
High phosphate - can’t excrete it
Low Active Vit D - can’t activate it
Low calcium – lack of vit D and high phosphate
Secondary PTH - due to all 3 above, ^osteoclast
Osteomalacia: vit D def, increased bone turnover without enough calcium
Osteosclerosis: compensatory osteoblast^ but not mineralised properly
Rugger jersey spinal XR (sclerosis of ends of vertebral body, malacia in centre)
-> v phosphate in diet, phosphate binders (SE: ^Ca, vascular calcification), vit D (alfacalcidol), parathyroidectomy
Common Nephrotic syndromes
Minimal change
Membranous
Focal segmental GS
Diabetic
Amyloid
Common nephritic
Rapidly progressive GN
IgA nephropathy
Alport
Overlap - Diffuse proliferative, membranoproliferative and post strep
Extra renal manifestations of PKD
Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian cysts
MR
Colonic diverticula
Aortic root dilatation, dissection
Abdominal wall hernia
AKI Staging
Diagnose if
^creat by 26+ in 48hrs OR ^creat by 50%+ in 7 days OR urine output <0.5ml/kg/hour for >6hrs
Staging
1 - creatinine increase ≥ 1.5-1.9 x baseline OR urine <0.5ml/kg/hr for 6 hours
2 - creatinine ≥ 2-2.9 x baseline OR
urine <0.5ml/kg/hr for 12 hours
3 - creatinine ≥ 3 x baseline OR
creatinine increase to ≥ 354 OR
urine <0.3ml/kg/hr for 24hrs OR
RRT
CKD - classification
1) eGFR >90 (must be other evidence of damage e.g., U&Es/ proteinuria)
2) 60-90 + other evidence
3a) <60
3b) <45
4) <30
5) <15 (failure - need dialysis or transplant)
eGFR based on serum creatinine, age, sex, ethnicity
- effected by pregnancy, muscle, red meat
CKD - Extras
HTN
-> ACEi (investigate if GFR reduces >25% or creatinine rises >30%), furosemide
Proteinuria
Albumin: creatinine, first pass morning
-> refer 70+ or 30 + haematuria, ACEi and SGLT2 inh
Most CKD patients have bilaterally small kidneys (excl. early DM, PCKD, amyloid)
Diabetic Nephropathy
Annual albumin: creatinine (early morning)
-> ACEi if 3+, v protein, control glucose, statins
BP drugs if >135/85 (or 130/80 in T1 w/ albuminuria)
- aim for 140/90
