Kidneys

Question 1

top 3 most common causes of AKI

Answer 1

1) sepsis, 2) major surgery, 3) cardiogenic shock

(4) hypovolaemia, 5)drugs, 6) hepatorenal syndrome)

Question 2

What is the following:
a subset of acute renal railure due to acute, irreversible damage to the kidney parenchyma whether in the de novo acute setting or in addition to a previously existing kidney disease.

Answer 2

intrinsic renal failure

Question 3

name some risk factors for acute kidney injury

Answer 3

preexisting CKD/kidney impairment, age, male sex, comorbidity(cancer, cardiovascular disease, diabetes, hypertension etc)

Question 4

what 3 life-threatening conditions can arise due to AKI?

Answer 4

volume overload
hyperkalaemia
metabolic acidosis

Question 5

name the 4 principal prerenal causes of AKI

Answer 5

1) hypovolaemia (haemorrhage, vomiting, diarrhoea)
2) renal hypoperfusion(NSAIDs/selective COX 2 inhibs, ACE inhibs/Angiotension 2r blockers, AAA, renal artery stenosis/occlusion, hepatorenal syndrome)
3) hypotension(cardiogenic shock, distributive shock (anaphylaxis, sepsis)
4) oedematous states (cardiac failure, hepatic cirrhosis, nephrotic syndrome)

Question 6

name 4 drugs that can lead to renal hypoperfusion (pre-renal cause of AKI)

Answer 6

NSAIDs (e.g. paracetamol, aspirin, diclofenac, ibuprofen)
Selective COX 2 inhibitors (celebrex, celecoxib–>reduce risk of peptic ulceration)
ACE inhibitors (-prils, e.g. ramipril)
Angiotensin 2 receptor antagonists (ARBs) (losartan, candesartan, valsartan)

Question 7

name the 4 principal instrinsic (renal) causes of AKI

Answer 7

1) glomerular disease(inflammatory or thrombotic)
2) interstitial nephritis (drug induced, infiltrative, granulomatous, infection related)
3) tubular injury (ischaemia, toxins, metabolic, crystals)
4) vascular (vasculitis, cryoglobulinaemia, polyarteritis nodosa, thrombotic microangiography, cholesterol emboli, renal artery/vein thrombosis)

Question 8

name the 2 principal postrenal causes of acute renal failure

Answer 8

intrinsic(intraluminal, intramural)

extrinsic(pelvic malignancy, retroperitoneal fibrosis)

Question 9

what urinanalysis investigations are most useful in AKI?

Answer 9

Microscopy: red cell casts=glomerularnephritis
Dipstick: blood and/or protein on suggests inflammatory process

Question 10

What biochemistry investigations are most useful in AKI?

Answer 10

serial urea and creatinine= monitor progress
serial electrolytes= check for metabolic consequences of AKI, including hyperkalaemia, hpocalcaemia, hyperphosphataemia, and metabolic acidosis.
blood gases, serum bicarbonate= check for metabolic acidosis
creatine kinase, myoglobinuria= very high creatine kinase and myoglobinuria suggests rhabdomyalsis
C reactive protein=non specific marker of infection/inflammation
serum immunoglobulins, serum protein electrophoresis, Bence Jones proteinuria=immune paresis, monoclonal band on serum electrophoresis and bence jones proteinuria all suggest myeloma.

Question 11

What haematology investigations are most useful in AKI?

Answer 11

FBC, blood film=oesinophilia may be present in acute interstitial nephritis, or vasculitis. Thrombocytopenia and red cell fragments suggest thrombotic microangiopathy.
Coagulation studies= DIC associated with sepsis.

Question 12

what immunology investigations are most useful in AKI?

Answer 12

ANA(antinuclear antibodies) +ve in SLE and some other autoimmune disorders.
anti-dsDNA antibodies=specific for SLE
Prescence of :ANCA (antineutrophil cytoplasmic antibodies); also antiproteinase 3 (PR3) and antimyeloperoxidase antibodies (MPO) are alll assoc with systemic vasculitis.
Low complement concentrations (hypocomplementaemia)=low in SLE< acute postinfectious glomerulonephritis and cryoglobulinaemia.
antiglomerular basement(anti-GBM) antibodies=present in goodpasture’s disease

Question 13

what radiological investigation is most useful in AKI?

Answer 13

renal ultrasound scan=checks renal size, symmetry, and for evidence of obstruction.

Question 14

what are the 4 classifications of intrinsic renal failure?

Answer 14

1) glomerular-immune mediated (nephrotic syndromes), drugs
2) tubular-acute tubular necrosis, drugs
3) interstitial-pyelonephritis, autoimmune disease (e.g. SLE), malignancy
4) vascular-vasculitis, thromboembolic disease, malignant HTN

Question 15

what is the most common cause of intrinsic renal failure in hospital?

Answer 15

acute tubular necrosis (usually ischaemic).

Question 16

what leads to acute on chronic renal failure?

Answer 16

diabetic nephropathy
hypertension-related intrinsic renal failure
nephrotoxicity

Question 17

what do these 3 histological features appear in?

1) expansion of mesangium (due to hyperglycaemic accumulation of tissue)
2) thickening of GBM
3) glomerular sclerosis (due to intraglomerular hypertension)

Answer 17

diabetic nephropathy

Question 18

what leads to diagnosis of diabetic nephropathy?

Answer 18

A long-standing diabetic (type 1 or 2) develops all 3 of the following:

1) persistent albuminuria(more than 300mg/24 hours at least 2 occasions, 3-6 months apart)
2) progressive reduction of eGFR
3) hypertension

Question 19

what is the clinical presentation of diabetic nephropathy?

Answer 19

foamy urine
persistent proteinuria in a diabetic
diabetic retinopathy
fatigue
foot oedema assoc with hypoalbuminaemia
other diabetes assoc disorders (PVD, HTN, coronary artery disease)

Question 20

what is the difference between the management of type 1 and type 2 diabetics with diabetic nephropathy?

Answer 20

type 1= microalbuminuria in the early phase may be reduced with ACEi
type 2=most important goal is to achieve BP and blood sugar control ASAP.

Question 21

what are the four different ways in which glomerularnephritis can present?

Answer 21

nephritic syndrome (haematuria and some proteinuria)
nephrotic syndrome (no haematuria and lots of proteinuria)
AKI with mild hypertension
chronic nephritic syndrome(e.g. lupus, amyloid)

Question 22

what is the pharaoh mnemonic for nephritic syndrome?

Answer 22

Proteinuria
Haematuria
Azotaemia
RBC casts- 5 RBC/high powered microscope
Anti-streptoclysin O titres(if post-strep)
Oliguria
Hypertension (salt and water retention)

Question 23

Name 5 conditions that manifest as nephritic syndrome.

Answer 23

post-strep glomerulonephritis
rapid progressive glomerulonephritis
berger's disease (IgA nephropathy)
henoch-schonlein purpura
multiple myeloma

Question 24

Name 4 conditions that manifest as nephrotic syndrome.

Answer 24

minimal change disease
focal segmental glomerulosclerosis
membranous glomerulonephritis
membranoproliferative glomerularnephritis

Question 25

which 2 drug classes are absolutely contraindicated in renal artery stenosis?

Answer 25

ACE inhibitors and ARBs (angiotensin receptor blockers)

Question 26

disease that affected the small vessels of the kidneys predominantly. There is inflammatory infiltrate within the walls of vessels. It is classified by serological markers (is ANCA present/absent? Are there specific immune complexes involved?) Diagnosis is made as a last resort (rule out all other causes of symtoms).

Answer 26

vasculitis. Treatment=steroids. Small vessels vasculitudes: ``` ANCA-assoc: wegener's granulomatosis microscopic polyangiitis churg-strauss syndrome renal limited vasculitis ``` ``` non-ANCA assoc: goodpasture's syndrome cryoglobulinaemia lupus henoch-schonlein purpura ```

Question 27

nephritic syndrome presentation classically occurs after strep pyogenes infection immunofluorescence shows coarse granular IgG or C3 deposits labs show increased red cells and casts, increased ISO titer

Answer 27

post-streptococcal glomerulonephritis

Question 28

nephritic syndrome presentation goodpasture's disease is in this category immunofluorescence shows smooth and linear IgG deposits treat with prednisolone and plasmapharesis

Answer 28

rapidly progressive glomerulonephritis(aka crescentic glomerularnephritis)

Question 29

nephritic syndrome presentation IgA deposits in the mesangium presents with recurrent haematuria and low grade proteinuria 25% can progress to renal failure, otherwise harmless treat with prednisolone

Answer 29

berger's disease(aka IgA nephropathy)

Question 30

nephritic syndrome presentation always in children type of IgA nephropathy presents with abdo pain, GI bleed, vomiting and haematuria classically can find palpable purpura on buttocks and legs self-limiting disease, requires no steroids

Answer 30

henoch-scholein purpura

Question 31

``` nephritic syndrome presentation bence jones protein in the urine assoc with hypercalcaemia susceptible to encapsulated bacteria (due to defect in antibody production) treatment depends on the underlying type ```

Answer 31

multiple myeloma

Question 32

nephrotic syndrome presentation occurs in young children treat with prednisolone

Answer 32

minimal change disease

Question 33

nephrotic syndrome presentation similar to minimal change disease, but occurs in adults common in young, hypertensive males treat with prednisolone and cyclophosphamide

Answer 33

focal segmental glomerulosclerosis

Question 34

nephrotic syndrome presentation most common primary nephritic syndrome in adults slowly progressive disorder many causes (HBV, HCV, syphilis, malignancies, SLE) treat with prednisolone and cyclophosphamide 50% of cases progress to end-stage renal failure

Answer 34

membranous glomerulonephritis

Question 35

nephrotic syndrome presentation type 1 is slowly progressive, whilst type 2 is aggressive autoantibody against C3 convertase(low C3 levels) treat with prednisolone and plasmapharesis

Answer 35

membranoproliferative glomerulonephritis

Question 36

what are the 2 classifications of nephrotic syndrome?

Answer 36

``` primary glomerular disease (idiopathic), eg. minimal change disease, focal segmental glomerulosclerosis, etc. secondary disease(systemic disease (e.g. DM, SLE, amyloidosis), cancer (esp. membranous nephrotic syndrome), severe systemic infection. ```

Question 37

``` what syndrome is this? haematuria limited proteinuria slight oedema hypertension oliguria damage to podocytes, deposition of matrix ```

Answer 37

nephritic syndrome

Question 38

``` what syndrome is this? no haematuria proteinuria >3.5g/day (significant) gross oedema decreased albumin hypercoagulation hyperlipidaemia inflammation of glomeruli and blood vessels ```

Answer 38

nephrotic syndrome

Question 39

name the 5 functions of the kidneys.

Answer 39

1. excretion of waste products 2. regulation of acid-base balance (and water homeostasis) 3. endocrine functions (RAAAS, EPO, ADH-aldosterone complex) 4. metabolism of vit D and calcium 5. gluconeogenesis in fasting state (involving small molecular weight proteins)

Question 40

findings in urine microscopy when diagnosing type of renal failure: scant hyaline casts

Answer 40

pre-renal AKI

Question 41

findings in urine microscopy when diagnosing type of renal failure: many hyaline casts, RBC present.

Answer 41

post-renal AKI

Question 42

findings in urine microscopy when diagnosing type of renal failure: epithelial cells, muddy-brown, coarsely granular casts, WBCs present, low-grade proteinuria

Answer 42

Acute tubular necrosis

Question 43

findings in urine microscopy when diagnosing type of renal failure: WBCs and RBCs present, epithelial cells, eosinophils, low-moderate proteinuria

Answer 43

allergic interstitial nephritis

Question 44

findings in urine microscopy when diagnosing type of renal failure: RBC casts, dysmorphic red cells, moderate-severe proteinuria

Answer 44

glomerulonephritis

Question 45

what antibiotics are nephrotoxic?

Answer 45

aminoglycosides (gentamicin, neomycin, tsreptomycin). Act on gram -ve bacteria. Broad spectrum. Cause renal vasoconstriction. This can cause (ischaemic) acute tubular necrosis.

Question 46

``` which intrinsic renal disease does this indicate? eosinophilia haematuria pyuira(pus in urine) WBCs RBCs white cell casts ```

Answer 46

acute interstitial nephritis

Question 47

which intrinsic renal disease does this indicate? muddy brown, granular, epithelial cell casts tubular cells

Answer 47

acute tubular necrosis

Question 48

which intrinsic renal disease does this indicate? haematuria proteinuria dysmorphic RBCs

Answer 48

glomerulonephritis

Question 49

how do you distinguish between acute and chronic renal failure?

Answer 49

long duration of symptoms, nocturia, absence of acute illness, anaemia, hyperphosphataemia, hypocalcaemia= all suggest chronic renal failure (although similar findings can occur in AKI as complications). reduced renal size and cortical thickness on renal US scan=characteristic of chronic renal failure; however renal size is typically preserved in diabetics. BASICALLY: history and examination previous creatinine measurements, small kidneys on USS.

Question 50

how do you exclude diagnosis of obstruction as a cause of AKI?

Answer 50

-check for palpable bladder -ask about previous stones, and bladder outflow obstruction symptoms(weak stream, feeling of incomplete emptying, hesitancy) -renal US scan checks for renal dilatation and calyces; however obstruction can still be present without dilation (esp in malignancy). COMPLETE ANURIA=suggests renal tract obstruction BASICALLY: complete anuria?, palpable bladder, renal ultrasound

Question 51

how do you find out the patient's volume status?

Answer 51

hypovolaemia=postural hypotension and low venous pressure hypervolaemia=high venous pressure, pulmonary crepitations. ``` high levels of ADH-->increased tubular reabsorption of water and urea, and disproportionate rise in urea:creatinine ratio. increased catabolism(e.g. sepsis) also raises urea concentrations, as well as ingestion of protein (e.g. upper GI bleed) use of diuretics often makes interpretation of urinary indices uninterpretable. ``` BASICALLY=pulse, JVP, postural BP, daily weghts, fluid balance, disproportional increase in urea:creatinine ratio, urinary sodium concentration(unless on diuretics), fluid challenge(=rapid administration of fluid bolus to critically ill patient. Response to this must be assessed.)

Question 52

how do you check if other renal parenchymal disease exists (other than acute tubular necrosis)?

Answer 52

Ask about rashes, arthralgia, myalgia. Use of antibiotics and NSAIDs->can lead to acute interstitial nephritis. blood and urine on dipstick, as well as dysmorphic cells and red cell casts indicates glomerulonephritis eosinophils indicates acute interstitial nephritis BASICALLY: history and examination(systemic features?), urine dipstick and microscopy(red cells/red cell casts, eosinophils, proteinuria)

Question 53

how do you check if a major vascular occlusion has occured?

Answer 53

occlusion of normal renal artery=>loin pain and haematuria occlusion of previously stenosed renal artery=>can be asymptomatic, leaving the patient dependent on one functioning kidney. check for renal asymmetry on imaging: especialy when a patient is known to have vascular disease elsewhere. cholesterol embolism=> can occur after angiography/vascular surgery/anticoagulation/thrombolysis. Characterised by the classic triad of livedo reticularis (rash), acute renal failure, and eosinophilia. Onset 1-4 weeks post-intervention. BASICALLY: is there: atherosclerotic vascular disease, renal asymmetry, loin pain, macroscopic haematuria or complete anuria?