Nephrology AS cards Flashcards

Question

Definition of microalbuminuria?

Answer 1

30-300mg/24hr Earliest detectable sign of deterioration in DM Other causes: - HTN - minimal change GN

Answer 2

RBC, WBC or Tubular. RBC: glomerular haematuria WBC: Interstitial nephritis or pyelonephritis Tubular: ATN

Answer 3

- Haematuria, proteinuria, red cells/casts.

Answer 4

White cell casts, small protein, leucocyturia

Answer 5

- Synthesised during muscle turnover - Freely filtered and small proportion secreted by PCT - Increased muscle --> Increased creatinine: age, sex, race - Plasma Cr doesn't increase above normal until 50% increased in GFR

Answer 6

- Produced from ammonia by liver in ornithine cycle - Increased with protein meal (upper GI bleed or supplements) - Decreased with hepatic impairment - 10-70% is reabsorbed: depends on urine flow - Decreased flow --> increased urea reabsorption (in dehydration)

Answer 7

Decreased flow = Hypoperfusion/dehydration

Answer 8

Decreased filtration (renal failure)

Answer 9

- Vol of blood that can be cleared of a substance in 1min - CrC roughly approximates GFR as it is freely filtered and only a small proportion secreted (~10%) - Required urine concentration from 24hr collection - Can use radiolabelled EDTA: very rarely done.

Answer 10

- Modification of Diet in Renal Disease (MDRD) equation - CAGE = serum creatinine, age, gender, ethnicity! - Obvious need for urine collection.

Answer 11

- Validated for patients with established renal failure: ?applicable to general population - Most elderly people are in >stage 3 CFR by eGFR: may npt progress or impinge on their health. - eGFR is too pessimistic in mild renal impairment. - Factors which may affect the result = pregnancy, muscle mass, eating red meat 12 hrs prior to sample being taken. Higher creatinine in body builder = artificially lower eGFR.

Answer 12

Pre-renal - Shock - Renal vascular: RAS, - Toxins: NSAIDs, ACEi - Thrombosis - Hepatorenal syn

Answer 13

Glomerulonephritis Acute Tubular Necrosis Interstitial disease

Answer 14

``` Disease of renal papillae, pelvis, ureters, bladder or urethra. SNIPPIN - Stone - Neoplasm - INflammation: stricture - Prostatic hypertrophy - Posterior urethral valves - Infection: TB, schisto - Neuro: post-op, neuropathy ```

Answer 15

- Uraemia - Protein loss and Na+ retention - Acidosis - Hyperkalaemia - Anaemia - Vitamin D deficiency

Answer 16

``` Pruritis N/V Anorexia Lethargy Confusion restless legs Metallic taste Paraesthesia: neuropathy Bleeding Chest pain: serositis ```

Answer 17

``` Pale skin, Striae Pericardial/Pleural rub Fits Coma ```

Answer 18

Symptoms - Polyuria, polydipsia - Oliguria, anuria - Breathlessness

Answer 19

- Oedema - INcreased JVP - HTN (or decreased BP)

Answer 20

Breathlessness | Confusion

Answer 21

Kussmaul respiration?

Answer 22

Palpitations Chest pain Weakness

Answer 23

``` Peaked T waves Flattened P waves Increased PR interval Widened QRS Sine-wave pattern --> VF ```

Answer 24

``` Breathlessness Lethargy Faintness Tinnitus Aortic flow murmur ```

Answer 25

Pallor Tachycardia Flow murmurs (ESM @ apex)

Answer 26

Bone pain | Fractures

Answer 27

Osteomalacia - Looser's zones (pseudo #) - Cupped metaphyses

Answer 28

Bacteria in urine, symptomatic or asymptomatic

Answer 29

Symptomatic with +ve culture or dipstick

Answer 30

Symptomatic but no bacteriuria

Answer 31

- Uncomplicated: Normal GU tract + functioning. - Complicated: abnormal GU tract, outflow obstruction, decreased renal function, impaired host defence - Recurrent: further infection with new organism - Relapse: further infection with same organism

Answer 32

Pyelonephritis Cystitis Prostatitis

Answer 33

- Fevers, rigors - Loin pain and tenderness - Vomiting - Oliguria if ARF

Answer 34

- Frequency and urgency - Polyuria - Haematuria - Dysuria - Suprapubic tenderness - Foul smelling urine

Answer 35

- Flu-like symptoms* - Low backache - Dysuria - Tender swollen prostate on PR

Answer 36

Presence of leukocytes without infection - TB - Treated UTI - Appendicitis - Calculi - Tubulointerstitial nephritis - Papillary necrosis - Polycystic Kidney - Chemical cystitis (cyclophosphamide)

Answer 37

``` Female Sex Pregnancy Menopause DM Abnormal tract: stone, obstruction, catheter ```

Answer 38

- E.coli - Staphylococc Saprophyticus - Proteus (Struvite renal stones) - Klebsiella

Answer 39

- Dipstick - MSU for MCS - Bloods: FBC, U+E, Blood cultures (if systemic signs) - US: Children, men, recurrence, pyelonephritis

Answer 40

- 10^4 cfu/ml for most - Women with symptomatic UTI >10^2 cfu/l - Men >10^3 cfu/ml (if 80% of growth due to a single organism)

Answer 41

General: drink plenty of water Cystitis - Management for 3-6 days - Trimethoprim 200mg BD - Nitrofurantoin 50mg QDS (not in RF) - Causes lung fibrosis. - Cefalexin 500mg BD (good in RF) - Co-amoxiclav 625mg TDS

Answer 42

Cefotaxime/Ceftriaxone 1g IV BD for 10days No response: Augmentin 1.2g TDS + gentamicin. Gentamicin can cause an intrinsic AKI.

Answer 43

Drink more Abx prophylaxis ? Cranberry juice

Answer 44

- group of disorders resulting from glomerular damage - Can --> Proteinuria ± haematuria - Can --> AKI or ESRF

Answer 45

Asymptomatic haematuria Nephrotic syndrome Nephritic syndrome

Answer 46

Most common cause = Diabetes. - Deposition disease - Amyloidosis - Minimal change disease (child with nephrotic syndrome) - Focal and segmental glomerulosclerosis (may be idiopathic or secondary to HIV) - Membranous nephropathy (presentation: proteinuria/nephrotic syndrome/chronic kidney disease) - Membranoproliferative GN (generally mixed picture)

Answer 47

- Postinfectious GN - IgA nephropathy/ young adult with haematuria following URTI - Rapidly progressive GN (rapid onset, often presenting as acute kidney injury). Causes include Goodpasture's ANCA positive vasculitis. - Vasculitis (Wegener's + nose bleeds). - Anti-glomerular basement membrane (GBM)

Answer 48

Urinanalysis - Haematuria, proteinuria, dysmorphic RBC, leukocytes, RBC casts. Bence-Jones proteins. Bloods - Basic: FBC (anaemia) , U+E (elevted creatinine, liver enzymes for Hep B/C), ESR (ESR elevated) - Complement (C3 and C4) for immune complex GN - Abs: ANA, dsDNA, ANCA (pauci immune or anti-glomerular basement membrane) , GBM (GBM) - Serum protein electrophoresis and Ig - Infection: ASOT (post-strep) HBC, and HCV Imaging - CXR: infiltrates (Goodpasture's, Wegener's) - Renal US ± Biopsy

Answer 49

Refer to nephrologist Rx HTN aggressively (<130/80) Include ACEi/ARA.

Answer 50

1. IgA nephropathy 2. Thin BM 3. Alports

Answer 51

IgA nephropathy/Berger's Disease

Answer 52

- Young male with episodic macroscopic haematuria occuring a *FEW DAYS* after URTI - Rapid recovery between attacks. - increased IgA - Can occassionally lead to nephritic syndrome.

Answer 53

IgA Deposition in mesangium

Answer 54

If low risk of progression - supportive. If HTN or proteinuria develops - all patients should receive ACEi and ARBS. - Steroids or cyclophosphamide if decreasing renal function (6 months) - Prognosis = 20% ESRF after 20yrs.

Answer 55

- AD disease, commonest cause of asymptomatic haematuria -Features Persistent, asymptomatic microscopic haematuria. V. small risk of ESRF.

Answer 56

X-linked inheritance - Haematuria, proteinuria = progressive renal failure NOT APKD - Sensorineural deafness - Lens dislocation + Cataracts (lenticonus) - Retinal flecks - Females: haematuria only. Alport's patient with a failing renal transplant - caused by presence of anti-GBM anitbodies leading to Goodpasture's syndrome like picture. Can't see - Lenticonus Can't pee - CKD, hematuria Can't hear a high C - sensorineural deafness

Answer 57

- Haematuria (macro/micro) + red cell casts - Proteinuria --> Oedema (especially periorbital) - HTN - Oliguria and progressive renal impairment

Answer 58

- Proliferative/post strep | - Crescentic/Rapidly Progressive Glomerulonephritis.

Answer 59

- Young child develops malaise and nephritic syndrome with smoky urine - *1-2 WEEKS AFTER* sore throat or skin infection. - Delayed antibody-mediated syndrome. Pyelonephritis and a UTI would present differently including symptoms such as fever, dysuria and pain. - Present with headache, malaise, haematuria, proteinuria, HTN, Low C3, raised ASO

Answer 60

Increase ASOT Decreased C3 Biopsy shows: IgG and C3 deposition.

Answer 61

- Supportive management - Consider antibiotics - ACEi to treat proteinuira >1g/day Minority develop RPGN

Answer 62

Most aggressive GN which can lead to ESRF in a few days.

Answer 63

Type 1: Anti-GBM - (Goodpasture's) - 5% Presents with ***haemoptysis and haematuria*** Rare condition associated with pulmonary ahemorrhage and RPGlomerulonephritis. Factors increasing likelihood of pulmonary haemorrhage. - Smoking, LRTI, Pulmonary oedema, inhalation of hydrocarbons. Manage = plasma exchange, steroids, cyclophosphamide. Type 2: Immune Complex deposition (complication of any immune complex deposition = Berger's, post-strep, endocarditis, SLE) Type 3: Pauci Immune - 50% - cANCA: Wegener's (Granulomatosis with Polyangiitis) - pANCA: microscopic polyangiitis, Churg-Strauss - Even if ANCA+ve, may still be idiopathic: no features of systemic vasculitis

Answer 64

- Manage with Corticosteroids and other immunosuppressants. | - Manage CVS factors - lifestyle measures, statins, BP control.

Answer 65

- Proteinuria (>3.5g/24hr) - Hypoalbuminaemia (<30g/L) - Peripheral oedema (periorbital, genital, ascites, peripheral). - Hyperlipidaemia - Lipiduria Often intravascularly depleted with decreased JVP (CCF).

Answer 66

Same as glomerulonephritis - Basic bloods: FBC, U+E, ESR - Complement (C3 and C4) - Abs: ANA, dsDNA, ANCA, GBM - Serum protein electrophoresis and Ig - Infection: ASOT, HBC, HCV. All adults get biopsy. Steroids 1st with children: mostly minimal change.

Answer 67

- Hyperlipidaemia: increased cholesterol and triglycerides - Infection: decreased Ig, decreased complement activity - VTE: up to 40%. - Therefore prophylactic LMWH required. ***Due to loss of anti-thrombin III, protein C&S, rise in fibrinogen*** - Loss of thyroxine-binding globulin = low total, but not free, thyroxin level HIT.

Answer 68

DM: glomerulosclerosis SLE: Membranous - Present with proteinuria on urinalysis. Pre-eclampsia cannot occur before 20 weeks therefore cannot be possible. Can cause deranged TFTs due to urinary loss of thyroid-binding globulins, leading to a low total T4 level. Amyloidosis

Answer 69

1. Minimal change glomerulonephritis (common cause in children) - can be due to NSAIDs, Hodgkin's lymphoma, EBV. Offer prednisolone and only if poor prognosis then give biopsy. 2. Membranous Nephropathy (most common cause of adults - due to malignancy, but also diabetic nephropathy) 3. Focal Segmental GS 4. Membranoproliferative/ Mesangiocapillary GN/ Berger's/ IgA nephropathy.

Answer 70

- Commonest cause of nephrotic syndrome in children Causes: - URTI - infectious mononucleosis - drugs - NSAIDs, rifampicin - Hodgkin's lymphoma, thymoma - Biopsy: normal light micro, fusion of podocytes on EM - Management: Steroids (cyclophosphamide if steroid unresponsive) - Prog: 1% --> ESRF. 1/3 of patients have infrequent relapses and 1/3 of patients have frequent relapsed (2/3) with recurrent episodes.

Answer 71

``` 20-30% of adult nephrotic syndrome - Associations: Mainly malignancy Ca: lung, colon, breast Autoimmune: SLE, thyroiditis, rheumatoid Infections: HBV, malaria, syphilis Drugs: Penicillamine, gold, NSAIDs ``` On biopsy: Subepithelial immune complex deposits, basement membrane thickening on light microscopy. Subepithelial spikes on silver stain. Positive immunohistochemistry for PLA2 Management: - All patients should receive an ACEi or an ARB. - immunosuppression if renal functions declines. E.g steroid + cyclophospamide. Prognosis: 40% spontaneous remission.

Answer 72

If adult with nephrotic syndrome think focal segmental. - Commoner in Afro-Caribbeans - Common nephrotic syndrome in adults - Idiopathic or Secondary: VUR, Berger's, SCD, HIV. - Biopsy: focal scarring, IgM deposition - Management: Steroids or cyclophosphamide/cyclosporin - Prognosis: 30-50% --> ESRF (may recur in transplants).

Answer 73

- Rare - May lead to nephrotic or nephritic syndrome - Associated with HBV, HCV, Endocarditis - Prognosis: 50% --> ESRF

Answer 74

- Monitor U+E, BP, fluid balance, weight - Treat underlying cause: Majority are steroid-responsive. - Symptomatic/complication management: Oedema: Salt and fluid restrict + furosemide - Proteinuria: ACEi/ARA decreased proteinuria Increased lipids: Statin - VTE: Tinzaparin (risk of clotting) Management HTN.

Answer 75

Significant decline in renal function over hrs or days manifesting as an abrupt and sustained increased in serum urea and creatinine and/or a fall in urine output.

Answer 76

Pre-renal Renal Post-renal

Answer 77

- Shock (hypovolaemia, haemorrhage, sepsis, 3rd space filling) - renovascular compromise (NSAIDs, ACEi, bilateral renal artery stenosis + ACEi. In pre-renal urea:creatinine ratio indicated a pre-renal cause. Normally in pre-renal kidneys will try to hold onto sodium and there will be low fractional sodium excretion.

Answer 78

ATN: Ischaemia: shock, HTN, HUS, TTP Direct nephrotoxin: drug hypertensitivity

Answer 79

SNIPPIN - Stone - Neoplasm - Inflammation: Stricture - Prostatic hypertrophy - Posterior urethral valves - Infection: TB, Schisto - Neuro: Post-op, neuropathy

Answer 80

- Uraemia - Acidosis - Hyerkalaemia - Fluid overload Oedema, including pulmonary Increased BP (or decreased) S3 gallop Increased JVP

Answer 81

Can't tell for sure?: Manage as acute. Features of chronic AKI? - Hx of comorbidity: DM, HTN - Long duration of symptoms - Previously abnormal bloods (GP records)

Answer 82

- Postural hypotension - Decreased JVP - increased pulse - Poor skin turgor, dry mucous membranes

Answer 83

``` Suprapubic discomfort Palpable bladder Enlarged prostate Catheter Complete anuria (rare in ARF) ```

Answer 84

Associated with proteinuria±haematuria | Vasculitis: rash, arthralgia, nosebleed.

Answer 85

Bloods: FBC (anaemia, leucocytosis), U+E, (creatinine, potassium, urea), urea to creatinine ratio, LFTs, Glucose, Clotting, Ca, ESR ABG: hypoxaemia (oedema), acidosis, increased K+ GN screen: if cause unclear Urine dip: Dip, MCS, chemistry (U+E, PCR, Osmolality, BJP) ECG: Hyperkalaemia CXR: pulmonary oedema Renal US: renal size, hydronephrosis**** - must be done within 24h of assessment if no identifiable cause/ at risk of urinary tract obstruction NB: in pre-renal failure, urine is concentrated and Na is reabsorbed --> increased osmolality, Na <20mM.

Answer 86

RIFLE Classification - 3 grades of AKI and 2 outcomes - Classification determined by worst criteria

Answer 87

Risk: - Increased Cr x 1.5 - Decreased GFR >25% - UO: <0.5ml/kg/h x 6hr In the 1s

Answer 88

Injury: - Increased Cr x 2 - Decreased GFR >50% - UO: <0.5ml/kg/h x 12hrs In the 2s

Answer 89

Failure: - Increased Cr x 3 - Decreased GFR >75% - UO: <0.3ml/kg/h x 24hr, or anuria x 12hr. In the 3s

Answer 90

- Persistent ARF = complete LOF > 1month

Answer 91

- LOF >3 months.

Answer 92

- Identify and manage pre-renal or post-renal causes - Urgent US - Manage exacerbating factors: sepsis - Give PPI - Stop nephrotoxins: NSAIDs, ACEi, Gent, Vank - Stop meformin if Cr >150mM. Pre-renal - Volume expansion - Offer fluid 500ml 09% saline over 15mins. - Vasopressors (severe hypotension) - Diuretic if overloaded - Renal replacement therapy (haemodialysis) Manage hyperkalaemia.

Answer 93

Cathereise and monitor UO Consider CVP Fluid balance Weight

Answer 94

ECG feature (in order) - Peaked T waves - Flattened P waves - Increased PR interval - Widened QRS - Sine-wave pattern - VF

Answer 95

If K+ >6.5 or if there are ECG changes - Then admin - 10ml 10% calcium gluconate Protective effect begins in minute. - 100ml 20% glucose + 10u insulin (Actrapid) . - Salbutamol 5mg nebs (helps to lower potassium through intracellular migration of potassium). Removal of potassium from body - Calcium resonium - enemas are more effective than oral as potassium is secreted by rectum. - Loop diuretics - Dialysis Calcium resonium 15g PO or 30 PR Haemofiltration (usually needed if anuric)

Answer 96

- Sit up and give high-flow O2 - Morphine 2.5mg IV (±metoclopramide 10mg IV) - Furosemide 120-250mg IV over 1hr - GTN spray ± ISMN IVI (unless SBP <100) - If no response consider: CPAP Haemofiltration/haemodialysis ± venesection

Answer 97

Increased urea impaires haemostasis FFP + plats as needed Transfuse to maintain hb>10

Answer 98

- Persistent Hyperkalaemia >7mM - Refractory pulmonary oedema (as a result of volume overload). - Symptomatic uraemia: encephalopathy, pericarditis - Severe metabolic acidosis - Poisoning (e.g aspirin, methylglycol) AEIOU

Answer 99

Pre-renal: Shock or renovascular (HTN, GM, HRS) Renal: ATN, GN Post-renal: Obstruction, stone, neoplasm, catheter

Answer 100

- Presents in the context of critical illness - Uraemia - Hyperkalaemia - Acidosis - Oedema and increased BP

Answer 101

Resuscitate and assess fluid status - A: GCS increased may need airway management - B: pulmonary oedema - sit up, high flow oxygen - C: fluid status? CVS: Postural BP, JVP, HR Tissues: CRT, cold/warm hands, skin turgor, mucus membranes

Answer 102

- Hyperkalemia - Pulmonary oedema - Consider need for rapid dialysis Manage shock or dehydration - Fluid challenge 250-500ml over 30 mins - Repeat as necessary: aim for CVP of 5-10cm - Continue @ 20ml +UO/h

Answer 103

- Cardiac monitor - Urinary catheter - Consider CVP - Start fluid balance chart

Answer 104

Look for evidence of post-renal cause - Palpable ± tender bladder - Enlarge prostate/anuria, catheter - Hx Evidence of acute vs chronic = renal ultrasound = most patients with CRF have bilateral small kidneys. May also have hypocalcemia. - Ix Bloods, ABG, Urine dip, ECG, CXR, Renal US Manage sepsis Further management - Call urologists if obstructed despite cather.

Answer 105

Acute Intersitial/Tubulointerstital nephritis and eventually necrosis. - Immune mediated hypersensitivity with either drug or other Ag acting as haptans. Usually have rash, fever and eosinophilia. Can be due to penicillins. - ATN = Reversible or irreversible type of renal failure caused by ischaemic or toxic injury to the renal tubular epithelial cells. Injury results in cell death or detachment from basement membrane.

Answer 106

Ischaemia - Hypoperfusion, or kidney structural damage. Exogenous toxins - Nephrotoxins = intrarenal vasoconstriction, tubular toxicity (Aminoglycosides, amphotericin B, chemo drugs, NSAIDS. Endogenous toxins - Rhabdomyolsis (myoglobin) - this can be due to compartment syndrome producing myoglobinuria. Muddy brown casts. Leads to tubular cell necrosis. - Increased uric acid (gout) - Increased light chain proteins (myeloma).

Answer 107

Drug hypersensitivity in 70% - NSAIDS - Abx: ceph, penicillin, rifampicin, sulphonamides - Diuretics: frusemide, thiazide - Allopurinol - Cimetidine Infections in 15% - Staphs, Streps, hantavirus Immune disorders - SLE, Sjogren's, Sarcoid

Answer 108

Occurs 2* to prolonged renal ischaemia 2* to either continuing pre-renal injury or by direct toxicity 2* to sepsis or nephrotoxins - Oliguria - Hypotension - Tachycardia - Oedema - Orthopnoea/dyspnoea - granular/ tubular casts

Answer 109

- Fever, arthralgia - Rash - AKI --> Oliguria/Anuria - Uveitis - eosinophilia

Answer 110

- Increased IgE, Eosinohilia | - Dip: haematuria, proteinuria, WCC, IgE, esoniphils

Answer 111

- Urea + creatinine: raised urea/creatinine, hyperkalaemia, metabolic acidosis. - Elevated sodium in urine - Coagulation - Prolonged PTT

Answer 112

Stop offending drug | Prednisolone

Answer 113

Supportive care Stop drugs Manage volume

Answer 114

``` Fibrosis and tubular loss Commonly caused by: - Reflux and chronic pyelonephritis - DM - SCD or trait ```

Answer 115

- Prolonged heavy ingestion of compound analgesics - Often a Hx of chronic pain: headache, muscle pain. Features: - Sterile pyuria ± mild proteinuria - Slowly progressive CRF - Sloughed papilla can --> Obstruction + renal colic. Ix: CT w/o contrast (papillary calcifications) Rx: Stop analgesics

Answer 116

- AKI due to urate precipitation - Usually after chemo-induced cell lysis Rx: Hydration, urinary alkalinisation

Answer 117

- Diffuse renal parenchymal calcification - Progressive renal impairment - Causes: Malignancy Increased PTH Myeloma Sarcoidosis Vit D intoxification RTA

Answer 118

Those that are directly toxic --> Leading to ATN Those that cause hypersensitivity --> Tubulointerstitial nephritis

Answer 119

- NSAIDs - Antimicrobials: AVASTA - ACEi - Immunosuppresssants Ciclosporin Tacrolimus - Contrast media - Anaesthetics: enflurane DAMN drugs to be stopped in AKI - Diuretics - ACEi - Metformin (if Cr >150) - NSAIDs

Answer 120

- Aminoglycosides (Gent, Tobramycin) - Vancomycin - Acyclovir - Sulphonamides (trimethoprim) - Tetracycline (doxycycline) - Amphotericin

Answer 121

Myoglobin Urate Ig - eg light chains in myeloma

Answer 122

Skeletal muscle breakdown --> Release of: K+, PO4, urate Myoglobin, CK Increased K+ and AKI. Can also lead to DIC, renal failure.

Answer 123

> Ischaemia: embolism, surgery > Toxins: statins, fibrates, ecstasy, neuroleptics > Trauma: immobilisation, crush, burns, seizures, compartment syndrome, falls

Answer 124

- Muscle pain, swelling - Red/brown urine - AKI occurs 10-12hr later

Answer 125

Dipstick: +ve Hb, -ve RBCs. Bloods: Increased CK (increased 5x normal is diagnostic) , increased K, increased Po4, Increased Urate. Urine - Myoglobin increased in blood or urine.

Answer 126

- Manage hyperkalaemia - IV rehydration: 300ml/h to maintain good urine output - CVP monitoring if oliguria - IV NaHCO3 may be used to alkanalise urine and stabilise a less toxic form of myoglobin. ?Furosemide

Answer 127

- Kidney damage >3 months indicated by decreased function. - Symptoms usually only occur by stage 4 (GFR <30) - ESRF is stage 5 or need for RRT.

Answer 128

Stage 1 = GFR >90 (with some sign of kidney damage on other tests) - if all kidney tests are normal there is no CKD. Stage 2 = GFR >60-89 (with some sign of kidney damage) Stage 3a = 45-59 Stage 3b = 30-44 Stage 4 = 16-29 Stage 5 = <15

Answer 129

> 90--> <90 --> 60 --> 30 --> 15 If patient falls below eGFR of 30 or progressively by >15 in a year refer to a nephrologist.

Answer 130

- Renal artery stenosis - GN - Polycystic disease - Drugs: e.g analgesic nephropathy - Pyelonephritis: usually 2ndry to VUR - SLE - Myeloma and amyloidosis

Answer 131

Bloods: - Hb decreased - U+E (elevated creatinine), decreased GFR - ESR - Glucose - Decreased Ca/PO4 (AKI) If phosphate is high it is chronic. - Increased ALP - Increased PTH Urine - Microalbuminuria, proteinuria, haematuria. Protein:creatinine ratio - 300 means you are nephrotic. Immune: ANA, dsDNA, ANCA, GBM, C3, C4, Ig, Hep Film: burr cells

Answer 132

``` CXR: Cardiomegaly, pleural/pericardial effusion, oedema AXR: calcification from stones Renal US - Usually small (<9cm) - May be large: polycystic, amyloid ``` Bone X-rays: renal osteodystropy (pseudofractures) CT KUB: cortical scarring from pyelonephritis For contrast-enhanced CT - prevention of contrast induced nephropathy: volume expansion with 0.9% saline at a rate of 1mL/kg/hr for 12 hours pre- and post- procedure. Renal biopsy: if cause unclear and size normal

Answer 133

CRF HEALS - Cardiovascular disease - leading cause of death. - Renal osteodystrophy - Fluid (oedema) - HTN - Electrolyte disturbance - Anaemia - Leg restlessness - Sensory neuropathy

Answer 134

Osteoporosis: decreased mineral density Osteomalacia: Decreased mineralisation of osteiod 2ndry/3rdy HPT --> Osteitis fibrosa cystica - Subperiosteal bone resorption - Acral osteolysis: short stubby fingers - Pepperpot skull May get osteosclerosis --> Rugger Jersey spine = Sclerotic vertebral end-plate with lucent centre.

Answer 135

- Reduced 1a hydroxylase --> decrease vit D activation --> decreased Ca --> increased PTH. - Phosphate retention --> Decreased Ca and increased PTH - Increased PTH --> activation of osteoclasts ± osteoblasts - Also acidosis --> Bone resorption.

Answer 136

- Management of reversible causes - Stop nephrotoxic drugs Lifestyle - Exercise - Healthy weight - Stop smoking - Na, Fluid, PO4 restriction

Answer 137

- Statins - Low-dose aspirin - Manage DM Target for HTN (<140/90) - <130/80 if DM. In DM kidney disease give ACEi/ARB

Answer 138

Furosemide

Answer 139

Pathophysiology: - 1-alpha hydroxylation normally occurs in kidneys -> CKD leads to low Vit D - kidneys normally excrete phosphate but CKD -> high phosphate Other problems: > High phosphate level in CKD drags calcium from bones -> osteomalacia > low Ca - due to low vit D, high phosphate >2* hyperPTH - due to low Ca, high phosphate and low vit D Mx: > reduce phosphate intake > Phosphate binders: calcichew. As they are calcium based they can lead to hypercalcaemia symptoms. (Sevelamer is a non-calcium based phosphate binder.) > Vit D analgoues: calcitriol or Alfacalcidol. > Ca supplements/Cinacalcet: Ca Mimetics >parahytoidectomy may be needed in some ccases

Answer 140

Anaemia - Exclude IDA and ACD - EPO to raise Hb to 11g/dL epoetin alpha

Answer 141

Clonazepam

Answer 142

- Virology status: CMV, HCV, HIV, VZV, EBV - CVD - TB - ABO and HLA haplotype

Answer 143

Active infection Malignancy Severe HD or other co-morbidities

Answer 144

- Cadaveric: brainstem death with CV support - Non-heart beating donor :no active circulation - Live-related Optimal surgical timing HLA-match Improved graft survival - Live unrelated

Answer 145

Campath/alemtuzumab (anti-CD52)

Answer 146

- Prednisolone short-term and tacro-ciclo long-term

Answer 147

Hyperacute: due to pre-existent antibodies against donor HLA type 1 antigens (a type II hypersensitivity reaction) rarely seen due to HLA matching Post-op - Bleeding - Graft thrombosis - Infection - Urinary leaks Hyperacute rejection - ABO incompatibility - Thrombosis and SIRS

Answer 148

Acute Rejection - Increased Cr (± fever and graft pain) - appears like infection but sterile pyuria - confirm diagnosis on biopsy of transplanted kidney - Cell-mediated response - Responsive to immunosuppression.

Answer 149

- Interstitial fibrosis + tubular atrophy - Gradual increase in Cr and proteinuria - Not responsive to immunosuppression Initial management is steroid treatment - chronic rejection presents insidiously with deteriorating renal function.

Answer 150

Acute: reversible afferent arteriole constriction --> decreased GFR Chronic: tubular atrophy and fibrosis

Answer 151

Increased risk of infection: Opportunistic, fungi, warts Increased risk of malignancy: BCC, SCC, Lymphoma (EBV)

Answer 152

HTN and Atherosclerosis

Answer 153

- Rejection - Obstruction - ATN - Drug Toxicity

Answer 154

20% | Advanced/ESRF occurs in 40% of T1 and T2 DM.

Answer 155

- Diabetes nephropathy describes conglomerate of lesions occuring concurrently - Hyperglycaemia --> renal hyperperfusion --> hypertrophy and increased renal size. This is in constrast to chronic kidney disease where they have bilateral small kidneys. - Hypertrophy and metabolic defects including ROS production --> glomerulosclerosis and nephron loss. - Nephron loss --> RAS activation --> HTN

Answer 156

- Microalbuminuria (30-300 mg/d = (albumin: creatinine >2.5) Strong independent RF for CV disease. Therefore measure urinary albumin/creatinine ratio on a spot urine sample. If abnormal, repeat with a first-pass morning urine specimen. ACR should be used to screen nephropathy. Microalbuminuria is the EARLIEST clinically detectable sign of classic diabetic nephropathy. Rise in albumin loss to 30-300mg per day. - All diabetic patients require annual screening for albumin:creatinine ratio in early morning specimens. - Progresses to proteinuria (albuminuria >300mg/d) - Diabetic retinopathy usually co- exists and HTN is common

Answer 157

all patients should be screened annually using urinary albumin:creatinine ratio (ACR) should be an early morning specimen ACR > 2.5 = microalbuminuria

Answer 158

- Good glycaemic control delays onset and progression (keep HbA1c) - BP control below 130/80 - Start ACEi/ARB even if normotensive - Stop smoking (associated with reduced GFR) - Can use peritoneal dialysis or haemodialysis - Finally - consider pancreas-kidney transplantation.

Answer 159

- Renal involvement usually caused by AL/AA amyloid. - Features: - Proteinuria - Nephrotic syndrome - Progressive renal failure 55yr old with progressive weakness and dyspnea, hepatomegaly, proteinuria and worsening renal function. Commonly present with dyspnoea, hepatomegaly, proteinuria, worsening renal function.

Answer 160

- Large kidneys on US | - Biopsy

Answer 161

Primary target for AL. Monoclonal light chain assembles and deposits extracellularly, resulting in disruption of the glomerular basement membrane. AL produce immunoglobulin light chains - prone to misfolding from a native alpha-helical state into an insoluble beta-pleated sheet.

Answer 162

AA - Improper processing of serum amyloid A protein. - Rather than being broken down it cannot. - Commonly related to long-standing infections such as bronchiectasis, osteomyelitis, IBD.

Answer 163

Resembles idiopathic restrictive cardiomyopathy. Impairment in longitudinal functioning. Also causes conduction abnormalities.

Answer 164

Congo Red - demonstrates green birefringence when viewed under green birefringence.

Answer 165

``` Post Strep HCV HBV HIV SBE/IE Visceral abscess ```

Answer 166

HBV HCV Post-strep

Answer 167

Bacterial pyelonephitis CMV HBV Toxo

Answer 168

Renal infiltration: Leukaemia, lymphoma Obstruction: Pelvic tumour Mets Nephrotoxicity - Due to toxic chemo - Analgesics - Tumour Lysis Syndrome

Answer 169

Hyperparathyroidism --> hypercalcaemia Sarcoidosis --> increased Ca and TIN

Answer 170

Pathology - Excess production of monoclonal AB ± light chains (excreted and detected in 60% as urinary BJP) - Light chains block tubules and have direct toxic effects --> ATN - Myeloma also associated with increased Ca2+ (through stimulating osteoclastogenesis). Presentation - ARF/CRF - Amyloidosis Management - Ensure fluid intake of 3L/d to prevent further impairment - Dialysis may be required in ARF.

Answer 171

Rheumatoid SLE Diffuse Systemic Sclerosis

Answer 172

- NSAIDS --> ATN - Penicillamine + gold --> membranous GN - AA amyloidosis occurs in 15%

Answer 173

- Involves glomerulus in 40-60% --> ARF/CRF - Proteinuria + increased BP common - Management Proteinuria - ACEi Aggressive GN: immunosuppression

Answer 174

- Renal crisis: Malignant HTN + ARF (commonest cause of death) - Rx: ACEi if increased BP or renal crisis.

Answer 175

- Hypertension - Renal artery stenosis - Haemolytic Uraemic Syndrome - Thrombotic Thrombocytopenic Purpura

Answer 176

- Can be both cause and effect of renal damage - Renal diseases are commonest cause of 2ndry HTN (through activation of RAS, leading to retention of Na and water due to decreased excretion).

Answer 177

- Atherosclerosis in 80% - Fibromuscular dysplasia - Thromboembolism - External mass compression

Answer 178

- Refractory HTN - Worsening renal function after ACEi/ARB - Flash pulmonary oedema (no LV impairment on Echo)

Answer 179

- Bloods: Creatinine to estimate GFR, serum potassium for activation of RAS, should be low due to increased sodium. Aldosterone-to-renin <20 excludes primary aldosteronism. - ie if renin is high = RAS. - US + Doppler: small kidney + reduced flow - CT/MR angio - Renal angiography: gold standard.

Answer 180

E.coli 0157: h7 verotoxin --> endothelial dysfunction . Shiga Toxin This leads to cell damage, microvascular thrombosis and resulting MAHA (Microangiopathic haemolytic anaemia). Haemolysis, anaemia, thrombocytopenia, raised LDH, Urea and Creatinine raised. Ix - FBC = anaemia, thrombocytopenia, fragmented blood film - U&E = AKI - stool culture Management - Fluids, blood transfusion and dialysis. - No role for antibiotics. - Indication for plasma exchange in severe HUS usually when there is no diarrhoea present. - Eculizumab Different to TTP = neuro signs. DIC = pancytopaenia

Answer 181

Use medical treatment with CV risk factors. (Ue ACEi and attempt to keep HTN below 130/80). Use statin, antiplatelet (aspirin 2nd line: Then angioplasty + stenting. Consider when refractory HTN on >3 medications, progressive CKD, AKI on ACEi, flash pulmonary oedema, bilateral RAS. - Give post-stenting clopidogrel 3rd line: surgical reconstruction of renal arteries (eg when AAA involved)

Answer 182

- Young children eating undercooked burgers - Bloody diarrhoea + abdominal pain precedes: MAHA, thrombocytopenia, renal failure.

Answer 183

- Schistocytes (RBC fragments) and are seen in haemolytic anaemia - decreased platelets - decreased Hb, - Renal failure - Normal clotting (rule out other causes of thrombocytopenia such as DIC) - PCR for Shiga Toxin

Answer 184

- Usually resolves spontaneously - RBC transfusion - Dialysis or plasma exchange may be needed (if TTP) or eculizumab

Answer 185

Thrombotic Thrombocytopenic Purpura. - Clinical syndrome characterised by MAHA, thrombocytopenic purpura, renal failure, fever, CNS signs: confusion, seizures).

Answer 186

``` MAHA Thrombocytopenic purpura Neurological dysfunction Renal dysfunction Fever ```

Answer 187

May involve unusually large vWF multimers. | This may also be due to lack of ADAMTS-13 cleaving enzyme for von Willebrand factor.

Answer 188

1) Carrier protein for Factor VIII, protecting it from degradation. 2) Bridge connecting platelets to damaged endothelium. Large vWF leads to aggregation of circulating platelets at sites of high intravascular shear stress. This leads to thombi in the microvascular system.

Answer 189

- Blood: Platelets decreased, anaemia, - Smear: schistocytes, reticulocyte count raised, - Coombs: negative - Normal clotting

Answer 190

- Plasmapherisis/Plasma exchange - Immunosuppression (prednisolone/ Caplacizumab which interacts with vWF). If steroids unsuccessful use vincristine/rituximab/cyclophosphamide/ciclosporin. - Splenectomy - will need polyvalent pneumococcal vaccine, Hib, meningococcal.

Answer 191

Renal tubular acidosis - Type 1 (Distal) - Type 2 (Proximal) - Fanconi's syndrome - Hereditary Hypokalaemic tubulopathies

Answer 192

- Impaired acid excretion leads to a hypercholaraemic metabolic acidosis - Both --> RAS activation --> K wasting and hypokalaemia. (as potassium cannot be reclaimed)

Answer 193

- Inability to excrete H+, even when acidotic - Mutations of proton pump or moving bicarb into blood. - May complicate other renal disorders Either: - 1) hereditary - 2) AI: Sjorgen's, SLE, thyroiditis - 3) Drugs

Answer 194

- Hyperchloraemic metabolic acidosis + hypokalaemia - Urine alkalotic regardless of systemic acidosis. - Rickets/osteomalacia (bone buffering) - Renal stones and UTIs - Leading to nephrocalcinosis --> ESRF. This is because calcium stones have a propensity to form in alkaline urine.

Answer 195

- Diagnosis = Failure to acidify urine (pH >5.5) despite acid load. - Ix = serum bicarb, chloride, ABG, K. Management - Sodium alkali or potassium containing alkali solution.

Answer 196

Defect in HCO3 reabsorption in the PCT. Tubules can reabsorb some HCo3 so can acidify urine in systemic acidosis when HCO3 is reduced. - Usually associated wtih Fanconi Syndrome.

Answer 197

Diagnosis | Urine will acidify with acid load

Answer 198

Disturbance of PCT function -- > generalised impaired reabsorption. - Amino acids - k+ - HCO3 - Phosphate - Glucose

Answer 199

- Idiopathic - Inherited: inborn errors, Wilson's - Acquired: tubule damage (Drugs, myeloma)

Answer 200

- Polyuria - Hypophosphataemic rickets (vit D resistant) - Acidosis - Decreased K

Answer 201

Sodium alkali and/or potassium-containing alkali solution.

Answer 202

Bartter's Syndrome | Gitelman Syndrome

Answer 203

- Blockage of NaCL reabsorption in loop on Henle (as if taking furosemide) - Congenital salt wasting --> RAS activation --> hypokalaemia and metabolic alkalosis - Normal BP

Answer 204

- BLockage of NaCl reabsorption in DCT (taking thiazides) - COngenital salt wasting --> RAS activation --> hypokalaemia + metabolic alkalosis + hypocalcirua (due to increased Ca reabsorption) - Normal BP

Answer 205

AD PKD AR PKD Medularry Sponge Kidney Tuberous Sclerosis

Answer 206

Age - Adults 40-60 yrs Genetics - PKD1 on Chr 16 - PKD2 on Chr 14 Path - Large cysts arising from all parts of nephron - Progressive decline in renal function - 70% ESRF by 70yr.

Answer 207

- Mass: abdo mass + flank pain - Infected cyst - Stones - SBP increased - Haematuria or haemorrhage into cyst - Aneurysm: Berry --> SAH - Polyuria + nocturia - Extra-renal cysts:liver - Systolic murmur: Mitral valve prolapse

Answer 208

General - Increased water intake, decreased Na, Decreased Caffeine (may decreased cyst formation) - Monitor U+E, BP - Genetic counselling - MRI screen for Berry aneurysms

Answer 209

- Rx HTN aggressively: <130/80 ACEi best - Rx infection - Urine alkalinasation for nephrolithiasis

Answer 210

Pain may be helped by laparoscopic cyst removal or nephrectomy - ESRF in 70% by 70 yrs, therefore dialysis or transplant.

Answer 211

Prev: 1:40,000 Infancy renal cyst and congenital hepatic fibrosis

Answer 212

Multiple cystic dilatations of the CDs in the medulla - Typically presents in 20-30s - commoner in femals - often asymptomatic but predisposes to: Hypercalciruia, nephrolithiasis, recurrent UTIs and pyelonephritis Haematuria Renal function usually normal.

Answer 213

AD condition with hamartomas in skin, brain, eye, kidney. Skin: Nasolabial adenoma sebaceum, ash-leaf macules, peri-ungal fibromas Neuro: decreased IQ, epilepsy Renal: cysts, angiomyolipomas

Answer 214

- Polycystic kidney: ADPKD, ARPKD, TS - Hypertrophy 2nd to contralateral renal agenesis - Obstruction (hydronephrosis) - Neoplasia: RCC, myeloma, amyloidosis - Occlusion (renal vein thrombosis) - HIV associated - Systemic: early DM, amyloid.

Answer 215

This is a patient with end stage renal disease. The likely current mode of renal replacement therapy is a renal transplant as evidenced by a scar in the right iliac fossa with an underlying mass consistent with a kidney. The mass was ovoid, smooth and non-tender. I noted a matured radio-cephalic AV fistula in the left arm, which did not have any puncture marks that would suggest recent use. The current mode of renal replacement therapy appearance to be adequate as the patient is euvolaemic. I noted evidence of immunosuppression in the form a fine postural tremor that may be suggestive for tacrolimus use. The patient did not appear cushingoid. I could not identify a cause of the ESRF and would therefore like to take a history from the patient to enquire about risk factors for CKD, such as diabetes and HTN. To complete my exam - Request Urine Dip for glucosuria, which may suggest diabetes as the underlying case, or blood or protein whch may indicate an underlying glomerulonephritis. Request an ECG + exam CVS system, as CKD is an independent factor for IHD****

Answer 216

Asian patient - DM prick marks - Diabetes - Palpate kidneys - APCKD risk of ICH, HTN + family US renal screening. - Purpura - Vasculitis/SLE - Stroke/CABG - vascular disease

Answer 217

``` Tenderness/heat over graft = rejection ACTIVE RRT methods - suggests a failed graft. - Tesio catheter - Fistula - palpable bruit/sign of use - Tenchkoff catheter ``` Anaemia, fluid overload, uraemia signs = graft failure

Answer 218

``` Hiccups Pruritis Loss of appetite Malaise Lemon tinged skin ```

Answer 219

- Steroids - remember violacious striae - Ciclosporin - gum hypertrophy, tremor, Peripheral neuropathy, HTN - Azothioprine = Anaemia, liver fibrosis - Tacrolimus - DM, tremor - Increased risk of malignacy with all of them (Esp cutaneous) Skin and colorectal.

Answer 220

Caecal Malignancy (cachexia) Crohns -clubbing, EN, PG. Adenopathy Transplanted Kidney

Answer 221

When you need dialysis - Uraemia with complications - encephalopathy/pericarditis - Refractory hyperkalaemia - Refractory pulmonary oedema - Refractory Metabolic acidosis - Drugs

Answer 222

- Emergency: CVVHF (ITU) - filtrations (continuous veno-veno haemofiltration). Slower + a lot more gentle than dialysis. - Haemodialysis - 3x per week - Tesio line or fistula Risk of endocarditis (TR). More efficient. Regular filtration of the blodo through dialysis mahcine in hospital 3x a week for 3-5hrs. - Peritoneal dialysis: Continuous ambulatory peritoneal dialysis (CAPD) or automated. Can laso have APD (automated) - whilst patient is sleeping. 3-5 exchanges over 8-10hrs. If the patient has Crohn's won't be suitable. - Sclerosing peritonitis, Hyperglycaemia (makes diabetes worse) Renal transplant

Answer 223

Painless haematuria HTN, polycythaemia, hyperCa Stauffer syndrome: Cholestasis/HSM. Von-Hippel Lindau Tuberous Sclerosis

Answer 224

``` Site infection Endocarditis Stenosis at site Hypotension Cardiac arrhythmia Air embolus Anaphylactic reaction to sterilising agents Disequilibration syndrome ```

Answer 225

Peritonitis - most common cause is due to coagulase-negative staphylococcus. = Staph epidermidis. Staph A is another common cause. - Sclerosing peritonitis - Catheter infection - Catheter blockage - Constipation - Fluid retention - Hyperglycaemia - Hernia

Answer 226

``` DVT PE Opportunistic infections Malignancies Bone Marrow suppression Recurrence of original disease Urinary tract obstruction CVS Graft rejection ```

Answer 227

``` breathlessness fatigue insomnia pruritus poor appetite swelling weakness weight gain/loss abdominal cramps nausea muscle cramps headaches cognitive impairment anxiety depression sexual dysfunction ```

Answer 228

- 25-30ml/kg/day of water - 1mmol /kg/day of potassium, sodium and chloride. - k = max rate of K infusion via a peripheral line is 10mmol/hour on a standard ward. 40mmol of K over 4 hrs. - IN ITU may give it quicker - max 20 mmol/hr - 50-100g/day of glucose to limit starvation ketosis. Irrespective of glucose requirements. When administering NaCL - risk of hyperchloraemic metabolic acidosis.

Answer 229

Palpable purpuric rash Abdo pina polyarthritis features of IgA nephropathy (Haematuria, renal failure)

Answer 230

Continuous bladder irrigation is the treatment of acute clot retention. 3 way foley catheter.

Answer 231

urine dipstick is the test of choice for detecting haematuria - persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart - renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

Answer 232

Urgent referral (i.e. within 2 weeks) Aged >= 45 years AND: - unexplained visible haematuria without urinary tract infection, or - visible haematuria that persists or recurs after successful treatment of urinary tract infection Aged >= 60 years AND have unexplained - non-visible haematuria AND either dysuria or a raised white cell count on a blood test

Answer 233

Non-urgent referral Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection Since the investigation (or not) of non-visible haematuria is such as a common dilemma a number of guidelines have been published. They generally agree with NICE guidance, of note: patients under the age of 40 years with normal renal function, no proteinuria and who are normotensive do not need to be referred and may be managed in primary care

Answer 234

Haematuria >40 -=urology | Haematuria <40 = renal

Answer 235

1. ) Increased potassium loss: - Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics - GI losses: diarrhoea, vomiting, ileostomy - Renal causes: dialysis - Endocrine disorders: hyperaldosteronism, Cushing's syndrome 2. ) Trans-cellular shift - Insulin/glucose therapy - Salbutamol - Theophylline - Metabolic alkalosis 3. ) Decreased potassium intake 4. ) Magnesium depletion (associated with increased potassium loss)

Answer 236

- Mild to moderate hypokalaemia 2.5 - 3.4 mmol/l can be treated with oral potassium provided the patient is not symptomatic and there are no ECG changes. - Severe hypokalaemia (<2.5mmol/l) or symptomatic hypokalaemia should be managed with IV replacement. The patient should be managed in an area where cardiac monitoring can take place. If there are no contraindications to fluid therapy (e.g. volume overload, heart failure) potassium should be diluted to low concentrations as higher concentrations can be phlebitic. ***The infusion rate should not exceed 20mmol/hr.*** In this case, 3 bags of 1L 0.9% Saline with 40mmol KCL over 24hrs is the correct answer.

Answer 237

Pre-renal uraemia - <20 urinary sodium - >500 urine osmolality - <1% sodium excretion - Good response to fluid challenge - Raised urea/creatinine ratio In pre-renal = kidney's hold on to sodium to preserve volume. Acute tubular necrosis (damage to tubular cells due to prolonged ischaemia or toxins). - Kidneys can no longer concentrate urine or train sodium. - >40 mmol/L - <350 mOsm/kg - >1% - Poor response to fluid - Normal serum urea/creatinine ratio - fractional urea >35%

Answer 238

Kidneys inability to respond to vasopressin. Give the patient thiazide diuretic works as polyuria is a symptom of the disorder. Causes of nephrogenic DI > genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel > electrolytes: hypercalcaemia, hypokalaemia > drugs: demeclocycline, lithium > tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis Investigation - High plasma osmolality, low urine osmolality - a urine osmolality of >700 mOsm/kg excludes diabetes insipidus - water deprivation test Management - nephrogenic diabetes insipidus: thiazides, low salt/protein diet - central diabetes insipidus can be treated with desmopressin

Answer 239

``` idiopathic post head injury pituitary surgery craniopharyngiomas histiocytosis X DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome) haemochromatosis ```

Answer 240

6-8 weeks. The AV fistula causes arterialisation of the vein due to the high pressure of the artery. The shunted blood flow causes an increase in growth factors and further hypertrophy of the venous wall. It takes 6 to 8 weeks post-surgery to allow full maturation to take place where the fistula can withstand a dialysis flow rate of 500ml/min. Preferred method of access for haemodialysis.

Answer 241

- infection - thrombosis = may be detected by the absence of a bruit - stenosis = may present with acute limb pain - steal syndrome

Answer 242

Haematopoeitic growth factor that stimulates the production of erythrocytes. Treats CKD associated anaemia and improves exercise tolerance. DOes not improve renal function. Secreted by kidney in response to cellular hypoxia. Used to treat anaemia associated with CKD. SE: - accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients) - bone aches - flu-like symptoms = skin rashes, urticaria - pure red cell aplasia* (due to antibodies against erythropoietin) - raised PCV increases risk of thrombosis (e.g. Fistula) - iron deficiency 2nd to increased erythropoiesis

Answer 243

- iron deficiency - inadequate dose - concurrent infection/inflammation - hyperparathyroid bone disease - aluminium toxicity

Answer 244

Normal anion gap = hyperchloraemic metabolic acidosis Normal anion gap = 8-14. Causes of normal anion gap acidosis: [ABCD] - Addison's disease - this is because loss of aldosterone function, causing less sodium but increased potassium. The acidosis is also due to loss of aldosterone function, more Na excreted and more H+ retention. - Bicarbonate loss (GI): diarrhoea, ureterosigmostomy, fistula. - Chloride (ammonium) injection - Drugs e.g acetazolamide - Renal tubular acidosis Raised anion gap - Lactate: shock, hypoxia, sepsis or tissue ischaemia. - ketones: diabetic ketoacidosis, alcohol - Urate: Renal failure - Acid poisoning: salicylate, methanol. For salicylate poisoning - common presentation presenting with nausea, vomiting, tinnitus and headache. Hyperventilation and secondary resp alkalosis. Over 24hrs, progresses to a metabolic acidosis and hypokalemia. Management - if recent give activated charcoal. Significant overdose may require alkalinisation with IV sodium bicarb.

Answer 245

``` vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction) diuretics liquorice, carbenoxolone hypokalaemia primary hyperaldosteronism Cushing's syndrome Bartter's syndrome congenital adrenal hyperplasia ```

Answer 246

Respiratory acidosis may be caused by a number of conditions: - COPD - decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema - sedative drugs: benzodiazepines, opiate overdose

Answer 247

``` Common causes anxiety leading to hyperventilation pulmonary embolism salicylate poisoning CNS disorders: stroke, subarachnoid haemorrhage, encephalitis altitude pregnancy ```

Answer 248

Features - HTN - Recurrent UTIs - Abdo pain - Renal stones - Haematuria - CKD Extra-renal manifestation - Liver cysts (70%) - leads to hepatomegaly. - Berry aneurysms (8%) - CVS system: Mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilatation, aortic dissection - Cysts in other organs, pancreas, spleen and rarely thyroid, oesophagus, ovary Ultrasound is the screening test for adult PKD*** Genes are PKD1 and PKD2 which code for polycystin-1 and polycystin 2. Screening investigation is abdo ultrasound. US Diagnostic criteria - 2 cyst, unilateral or bilateral if age <30 - 2 cysts in both kidneys if aged 30-59 yrs - 4 cysts in both kidneys if aged >60 Management - Tolvaptan may be an option. - CKD stage 2 or 3. - Evidence of rapidly progressing disease.

Answer 249

25% increases in creatinine occurring within 3 days of the intravascular administration of contrast media. RF: - Known renal impairment (esp diabetic nephropathy) - Age >70 - Dehydration - Cardiac failure - Use of nephrotoxic drugs

Answer 250

Consider in a young female patient who develops AKI after initiation of an ACEi. In older patient suspect atherosclerosis of renal arteries. Fibromuscular dysplasia - proliferation of cells in the wall of arteries causing the vessels to bulge or narrow and commonly affects women. Classic description includes string of beads appearance. Feature - HTN, CKD or acute renal failure secnondary to ACEi. - Flash pulmonary oedema.

Answer 251

ACEi reduce GFR by causing vasodilation of efferent arteriole and reducing glomerular filtration. Diuretics have a nephrotoxic effect as they prevent fluid being reabsorbed into capillaries. Metformin is renally cleared and would risk causing a lactic acidosis. Low dose aspirin is safe.

Answer 252

Lethargy + arthraglia is a common presentation of HH. Cause of central insipidus. AR so skips generations. Grandmother has bloodletting.

Answer 253

Check U+E to look for underlying AKI. Both renal tracts may be compromised so important to look at creatinine to look for post-renal AKI.

Answer 254

Renal cell carcinoma - Haematuria, loin pain, abdo mass. - Pyrexia or unknown origin - Left varicocele - due to compression of left testicular vein (or right) - Endocrine effects - EPO secretion (polycythaemia), PTH hormone (hypercalcaemia), renin, ACTH - 25% have mets at presentation.

Answer 255

Primary and secondary aldosteronism can be differentiated by looking at the renin levels. If renin is high then a secondary cause is more likely - renal artery stenosis.

Answer 256

- Patients on loop diuretics - after exercise - during fever

Answer 257

- cancer (bladder - frank haematuria in >60Y is bladder cancer until proven otherwise, renal, prostate) - strones - BPH - prostatitis - urethritis - e.g. Chlamydia - renal causes - IgA nephropathy, thin basement membrane disease

Answer 258

- UTI - menstruation - vigorous exercise (normally settles after ~3d) - sexual intercourse

Answer 259

- Foods = beetroot, rhubarb | - Drugs = rifampicin, doxorubicin

Answer 260

Check calcium if hypocalcaemia - more likely to be chronic Renal failure -> reduced metabolised 1,25OH-2D = reduced calcium reabsorption in kidneys

Answer 261

Common: - diuretics, caffeine, alcohol - DM - Lithium - Heart failure Infrequent: - Hypercalcaemia - hyperthyroidism Rare: - chronic renal failure - primary polydipsia - hypokalaemia Very rare: - diabetes insipidus

Answer 262

FIRST 10kg = 100ml/kg SECOND 10kg = 50ml/kg EVERY OTHER kg = 20ml/kg

Answer 263

Micturating cystography

Answer 264

- caused by recurrent UTI in young children - urine flows backwards from bladder towards kidneys - over time causes scarring - renal scar -> increased renin -> HTN - strong genetic disposition Ix = micturating cystogram

Answer 265

A rare but serious complication of haemodialysis -> cerebral oedema (mechanism unclear) Features = headache, drowsiness

Answer 266

According to serum creatinine change ± production of urine ``` 1 = Cr rise by 1.5-1.9x baseline = urine <0.5ml/kg/hr for >6h 2 = Cr rise <3x baseline = urine <0.5ml/kg/hr for >12hr 3 = Cr rise >3x baseline or >354 = urine <0.3ml/kg/hr for >24h or anuric for 12h ``` Pt deemed in stage 3 AKI if commenced on RRT irrespective of urine/ creatinine.