Renal Flashcards
(18 cards)
AKI:
- Definition
- Describe stages
- Risk factors (7)
- Symptoms
- Signs
- Causes
- Investigations
- Management
- Drugs to stop as inc risk of toxicity
- Complications (4)
AKI:
- Definition: >50% serum creatinine increase in 7 days or increase by 26.5 mmol in 48 hours or urine <0.5 in >6 hours
- Describe stages:
Stages 1: serum creatinine inc by 1-1.9 or >26.5. Urine output <0.5ml/kg/hr for 6-12 hours
Stage 2: 2-2.9. Urine output <0.5 for 12 hours.
Stage 3: >3x or >353.6. <0.3 for 12 hours
- Risk factors (7): ckd, diabetes, htn, sepsis, age, acei/nsaids/aminoglycosides/diuretics, contrast use
- Symptoms: n+v, flank pain, sob (pulmonary oedema), confusion
- Signs: oligouria, peripheral oedema, arrhythmias
- Causes
Prerenal: sepsis, renal art stenosis (atherosclerosis), haemorrhage, ccf, nsaids (dec prostag induced aff art dilatation)
Renal: acute tubular necrosis, acute intersistial nephritis, vasculitis, glomerulonephritis, rhabdomyolysis, TLS
Post renal: strictures, stones, tumour, retroperitoneal fibrosis, BPH - Investigations: urine dip, urine pcr, urine alb: creatinine, fbc/crp/u+es/bone profile, uss within 24 hours if no identifiable cause
- Management: remove drugs, treat cause, iv fluids or furosemide, monitor urine + bloods
- Drugs to stop: metformin, lithium, digoxin
- Complications (4): hyperkalaemia, fluid overload, metabolic acidosis, uraemia (encephalopathy + percarditis) = RRT
Nephrotic syndrome (glomerulonephritis):
- Definition
- Signs
- Causes (7)
- Complications (5)
- Management
Nephrotic syndrome (glomerulonephritis):
- Definition: podocyte damage leading to glomerular barrier charge dysfunction so proteins leak, reducing plasma oncotic pressure causing subsequent oedema
- Signs: proteinuria >350 (frothy urine), oedema, hypoalbuminaemia (<30), hypercholesterolaemia
- Causes (7)
1. minimal change disease: <6 years when podocytes fuse with foot processes. Can be idiopathic, nsaids/rifampicin/NHL/EBV. Needs corticosteroids
2. membranous: damaged podocytes causes sclerosis + deposits so thickening (spike + dome appearance on electron microscopy after biopsy). Can be idiopathic due to anti phospholipase ab, malig,, syphilis, sle etc. Needs acei + immunocomp + anticoags if v severe. Good indicators if f, young, assymp
3. focal segmental: igG + complement deposits = sclerosis. Can be idiopathic or due to other renal pathology, hiv, heroin, sickle cell, alports. Needs steroids.
Secondary: diabetic, sle, amyloidosis, nsaids
- Complications (5): thrombosis (loss proteins c/s + antithrombin 3) , infection (igs lost in urine), ckd, htn, hyperlipidaemia, hypocalc
- Ix: urine dip + MSU, urine albumin: proteinuria, fbc/clotting/u+es
- Management: acei (proteinuria), statins (hyperchol), diuretics (oedema), lmwh if albumin <20, treat cause
Nephritic syndrome (glomerulonephritis):
- Definition
- Signs
- Causes (7 - give associations, investigations and treatment)
- Management
Nephritic syndrome (glomerulonephritis):
- Definition:
- Signs: reduced egfr, haematuria, htn
- Causes (7 - give associations, investigations and treatment)
1. IgA nephropathy (bergers): most common glomerulonephritis + overlap with HSP. can be idiopathic or few days after urti/gi infection. Causes assymptomatic microhaematuria or visible, inc igA. Biopsy shows mesangial igA deposits in glomeruli. Needs acei/arb if protenuria 500-1000. If visible haematuria good prognosis. Bad if male, proteinuria, htn, smoking, hyperlipidaemia
2. Goodpastures: type 2 hypersens HLADR2 reaction where ab against type 4 collagen on bm in pulmonary + kidney. Anti gbm ab, pul infiltrates on cxr (+ haemoptysis). Biopsy shows linear igG deposition along bm. Needs plasma exchange + immunosupp
3. Post streptococcal: type 3 hypersens few weeks after group A b-hemolytic strep infection (tonsillitis, impetigo) usually in children. + anti strep ab, low c3. Biopsy shows IgG + igM + c3 deposits (subepithelial humps) and starry sky appearance on immunofluorescence. Self limiting, acei/arb, low na diet
4. Rapidly progressive: rapid loss in renal function via goodpastures, wegeners granulomatosis, sle etc. Formation of epithelial crests.
5. Vasculitis: small vessel ANCA
- granulomatosis w polyangitis: pul + nasopharyngeal involvement. cANCA + segmental necrotising gn on biopsy
- microscopic polyangitis: mild resp symptoms. pANCA + seg necrot on biopsy
- Eosinophilic gran w polyan: asthma, rhinitis, purpura, peripheral neuropathy. pANCA + focal seg nec.
6. Alport syndrome: x linked auto dom mut in type 5 coll. Presents in childhood with also bilat sensourineal deafness. Biopsy shows splitting of bm and alternating thickening and thinning of bm (basket weave). Can lead to goodpastures.
7. Lupus nephritis: can also be nephrotic.
- Management: low salt/water if overloaded
CKD:
- Definition
- Describe stages
- Causes (8)
- Risk factors
- Symptoms
- Investigations
- Management (4)
- Complications (8) and treatments of those complications
CKD:
- Definition: >3 months of kidney function reduced
- Describe stages: via egfr (creat, age, gender, ethnic - but can be affected by preg/muscle/red meat) + alb: creatinine ratio (marker of proteinuria)
- Causes (8): diabetes, htn, chronic glomerulonephritis, pckd, obstructive nephropathy, renovascular disease, chronic pyelonephritis, nsaids/ppi/lithium
- Risk factors: age, htn, diab, smoking
- Symptoms: assymp, fatigue, reduced appetite, nausea, pruritis (due to uraemia), oedema, peripheral neuropathy, htn
- Investigations: u+es, urine alb: creatinine, renal uss
- Management (4)
1. treat underlying cause
2. treat complications
3. treat progression: acei for proteinuria, bp control, monitor bloods
4. reduce cvs risk: statin 20mg, anti htn, smoking/weight etc
- Complications (8) and treatments of those complications
1. metabolic acidosis
2. hyperkalaemia
3. uraemia (pericarditis, encephalopathy)
4. bone mineral disease: dec vit d activation means dec ca absorption (hence high pi) in intestines so hypocalc causes inc pth (2ndary) which increases clast activity which softens bones causing malacia - needs vit d, ca and reduced pi in diet/pi binders and bisphosphonates
5. anaemia of chronic disease (normocytic) : reduced epo production means decreased rbc production, also blood loss, also reduced iron absorption (inc hepcidin levels) - needs erythropoiesis stimulating agents (SE: bone aches, flu, skin rash, inc risk thrombosis), oral iron if not
6. cvs disease - anaemia predisposes to LV hypertrophy
7. malnutrition
8. tertiary hyperparathyroidism: pth continues to increase and then so does ca leading to parathyroid gland hyperplasia - needs calcimimetics
remember primary hyperparathy (inc pth, inc ca, dec pi most likely due to adenoma so needs parathyroidectomy or calcimimetics)
Hypertensive nephropathy:
- Definition
- Investigations (5)
- Treatment
Hypertensive nephropathy:
- Definition: either due to advanced renal disease or htn causes nephroscoliosis
- Investigations (5): 24 hour urine catecholamines, ald: renin, dexameth suppression test, tsh, renal art stenosis
- Treatment: anti htn
Diabetic nephropathy:
- Definition
- Investigations
- Treatment
Diabetic nephropathy:
- Pathophy: due to glomerular damage, isch of eff/aff art. Initially excess glucose binds to proteins in efferent inc pressure hence inc egfr but then glomerulosclerosis causes thickening
- Investigations: annual ACR screening early morning
- Treatment: restrict protein, tight glycemic control, bp <130/80 control, acei if ACR >3
Polycystic kidney disease PCKD:
- Inheritance
- Pathophysiology
- Symptoms
- Extra renal manifestations (5)
- Investigations
- Management
- Complications (7)
Polycystic kidney disease PCKD:
- Inheritance: auto dom of PKD1/2
- Pathophysiology: causes cysts in parenchyma which impairs function + haemorrhage
- Symptoms: 40 yr old presents (or young if trauma) with htn + loin pain, haematuria, fever, bilateral palp kidneys, recurrent utis
- Extra renal manifestations (5):, mitral regurg, diverticula, ckd, cerebral berry aneurysms (SAH), cysts also in spleen/pancreas/liver/ovary
- Investigations: genetic, uss, if SAH in relative CT head
If fx then uss - diagnostic if 2 cysts <30yrs, 2 cysts in both kidneys 30-59, 4 if both >60
- Management: avoid contact/nsaids/anticoags. tolvaptan (ADH rec antag dec development cysts) only if ckd 2/3/rapidly progressing, antihtn, analgesia, abx/cyst drain, dialysis
- Complications (7): sah, ckd, chronic loin pain, htn, gross haematuria, renal stones, esrf
Renal replacement therapy:
- Indications (5)
- When to do active conservative management
- indications: metabolic acidosis, uraemia, ckd5, pulmonary oedema, electrolyte imbalance. life expectancy 6 mnths if not.
- conservative: if >80 + WHO score over 4
RRT - Peritoneal dialysis:
- How does it work
- Types (3)
- Advantages (2)
- Disadvantages (4)
- Complications (4)
RRT - Peritoneal dialysis:
- How does it work: dextrose into peritoneal cavity causes solutes across peritoneal membrane into fluid then removed
- Types (3): automated, continuous, assisted
- Advantages (2): inv qol, first choice
- Disadvantages (4): technical aspects, ultrafiltrate failure, peritonitis (staph epidermidis, aures so add vancomycin + ceftazidime to fluid), unsuitable if stoma/surgery
- Complications (4): hernia, peritoneal sclerosis, hydrothorax, drainage problems
RRT - Haemodialysis
- How does it work
- Types (3)
- Advantages (2)
- Disadvantages/complications (8)
RRT - Haemodialysis
- How does it work: tunnelled catheter into jugular vein or av fistula then pumps into dialyser which removes waste. 4hrs day 3x week. AV fistula usually radiocephalic is connection to increase pressure but takes 6-8 weeks to work (inc risk thrombosis, infection, stenosis)
- Types (3): home, nocturnal, contin
- Advantages (2): efficient, staff support
- Disadvantages/complications (8): sepsis, avf steal syndrome (limb distal to fistula becomes ischaemic), secure access, haemodynamic instability, muscle cramps, haemolysis, SVCO
RRT - Renal transplant:
- Advantages (2)
- Disadvantages (6)
- Contraindications (7)
- Types of donor
- Induction treatment
- Maintenance treatment
- Long term monitoring (6)
- Complications
RRT - Renal transplant:
- Advantages (2): normal life, dec mortality
- Disadvantages (6): rejection, lifelong immunosuppressants, strict criteria, inc malig risk, inc risk infection, long waiting list
- Contraindications (7): short life expectancy, non adherence, substance abuse, reversible renal disease, severe heart/lung disease, infection/malig
- Types of donor: living related, living unrelated (liver-donor, deceased donor, liver doner chain, altruistic), deceased
- Induction treatment: methylpred w basiliximab + thymoglobulin
- Maintenance treatment: pred, calcineurin inhib (tacrolimus, cyclosporin), antimetabolites (mycophenolate, azathioprine)
- Long term monitoring (6): egfr, cn1, proteinuria, ca/pi/pth, lipids, glucose, vaccinations, malig annual skin checks, contraception for 1 yr, cvs (tacro + ciclo can cause htn/hyperglyc/hyperlipid)
- Complications: <4 weeks - normal donor infection. 1-12 months - latent or community infections (CMV most common). >12 community. Diabetes
rejection - if acute needs removal. if <6 months may be reversible with steroids/immunosuppressants.
Type 2 hypersensitivity reaction:
- How long
- What cells are involved
- What do the cells cause
Type 3 hypersensitivity reaction:
- How long
- What cells are involved
- What do the cells cause
Acute interstitial nephritis:
- causes
- symptoms
- ix
Acute interstitial nephritis:
- causes: penicillin, rifampicin, nsaids, allopurinol, furosemide, sle, sarcoidosis, sjogrens
- symptoms: fever, rash, arthralgia, eosinophilia, mild renal impairment, htn
- ix: sterile pyuria, white cell casts
Rhabdomyolysis:
- causes
- symptoms
- mx
Rhabdomyolysis:
- causes: seizure, fall, ecstasy, statins
- symptoms: aki (v high creatinine), inc CK >5x, myoglobinuria, hypocalc (myog binds ca), inc pi, hyperkal, met acidosis
- mx: iv fluids, urinary alkalinisation
remember if ck not raised >5x think exercise induced ck elevation
Hemolytic uraemic syndrome:
- causes
- symptoms
- ix
- mx
Hemolytic uraemic syndrome:
- causes: ecoli producing toxin shigella, pneumococcal, hiv, sle
- symptoms: AKI, thrombocytopenia, microang hemolytic anaemia
- ix: fbc (anaemia hb <8 w neg coombs test, thrombocyt), u+es, stool culture, blood film (schistocytes + helmet cells)
- mx: fluids, blood, dialysis
Anion gap:
- equation
- normal gap + met acidosis causes
- inc gap + met acidosis causes
Met alkalosis causes
Anion gap:
- equation: Na + K - bicarb + cl
- normal gap + met acidosis causes: diarr, renal tubular acidosis, acetazolamide, addisons
- inc gap + met acidosis causes: inc lactate in shock, dka, urate in renal failure, acid poisoning
- met alk: vomiting, diuretics, hypokal, cushings, prim hyperald, CAH
- resp acidosis: copd, sedatives
- resp alkalosis: hypervent, pe, salicylate poisoning, cns disorders, preg
Acute tubular necrosis:
- causes
- causes: ischaemia (shock, sepsis), nephrotoxins (aminoglycosides, myoglobin, contrast, lead)
- aki features, muddy brown casts in urine, poor response to fluid challenge
