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3b > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Components of eGFR

A

Creatinine

Age, Gender, Race (Weight)

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2
Q

Creatinine
What
Cr vs eGFR

A

Chemical waste product from muscle metabolism (Muscley people have lots)

Therefore Cr clearance is > GFR - Because secreted as well as filtered!
Therefore inhibitors of secretion will make Cr rise and function look worse e.g. trimethoprim

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3
Q

Volume control
Aldosterone
Angiotensin II
ANP

A

Aldosterone (adrenal) -> decreased excretion
Angiotensin II -> decreased excretion
ANP - released by heart in response to high pressure -> increases excretion

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4
Q

Renal blood pressure control

A

Via volume control and vasoconstriction
Decreased BP at afferent arteriole -> juxtaglomerular apparatus -> renin
Prostaglandin - Preferentially dilates afferent arteriole
Angiotensin II - Preferentially constricts efferent arteriole (maintain GFR)
Antihypertensives -> ACEI (e.g. ramipril) and ARB (e.g. losartan)

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5
Q

ACE inhibitors
Indications
Dose
Side effects (4)

A

HTN, heart failure, post MI

Ramipril - start on 1.25/2.5mg PO OD at night

May impair renal function: decrease GFR (avoid NSAIDs), hyperkalaemia (avoid K+ spare diuretics)
Postural hypotension
Bradykinin mediated dry cough
Fatigue

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6
Q 
Angiotensin receptor blockers
Mechanism 
Indications 
Dose
Side effects (3)
A

Modulation of RAAS, similar to ACEI but no dry cough

HTN, heart failure, diabetic nephropathy

Losartan - usually 50mg PO OD, elderly =- 25mg PO OD

Renal impairment
Postural hypotension
Hyperkalaemia

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7
Q

Location of Sodium reabsorption

A

PCT (70%)

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8
Q

Potassium control

A

Potassium freely filtered at proximal tubule and loop of henle
Distal secretion determines renal excretion (Na, aldosterone driven)

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9
Q

Hypokalaemia meds

Hyperkalaemia meds

A

Loop diuretics, thiazide diuretics

Spironolactone, amiloride, ACEI, ARB

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10
Q

Hormones functions the kindey, function & physiology

A

Erythropoietin stimulates RBC production
Renal cortex acts as an O2 sensor; blood flow and oxygen requirement matched.

1-alpha hydroxylation of vitamin D
@proximal tubule calcitriol increases Ca and PO4 absorption from gut and suppresses PTH
*This process is inhibited by FGF-23 which is increased in CKD

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11
Q

Effects of angiotensin II (5)

A 
Increase sympathetic activity
Increase aldosterone secretion
Increase ADH secretion 
Tubular Na Cl and H2O re absorption. K excretion (aided by aldosterone)
Arteriole constriction.
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12
Q

Mechanism of
Spirolactone
Furosemide
Thiazides

Effect of BP/Na/K

A

Competitive binding of aldosterone receptor

Blocks Na/Cl/K pump in ascending limp of henle

Blocks Na/Cl pump in DCT

All cause hypotension/natremia/kalaemia (besides Spiro)

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13
Q

Fanconi syndrome

A

Generalised dysfunction of renal proximal tubule -> urinary loss of bicarb, glucose, aa, phosphate, peptides, organic acids. Leads to salt wasting and volume depletion

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14
Q

Types of renal tubular acidosis and findings (4)

A

Type 1: classic distal RTA
AD or AR mutations of proton pump. Inability to excrete H+ in distal tubules.
Min urine pH > 5.5, stones, serum potassium low-normal, plasma bicarb < 10

Type 2: inherited isolated proximal
Mutation of sodium bicarbonate cotransporter that transfers bicarb back to peritubular capillary. Inability to reabsorb bicarbonate
Min urine pH < 5.5, serum potassium low-normal, plasma bicarb < 12-20

Type 4: hyperkalaemic distal
Hyperkalaemia inhibits production of ammonia and decreases urine buffering capacity
Min urine pH < 5.5, serum potassium high, plasma bicarb > 17

Fanconi’s syndrome: Myeloma proteins and various drugs cause proximal tubule injury and proximal RTA, or AD inherited, bicarb <18

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15
Q

Presentation of RTA

A

Growth retardation/failure to thrive (children)
Muscle weakness (Fanconi)
Hypoglycaemia after fructose
Rickets (Fanconi and Type 2 proximal have persistent phosphate loss)
Distal RTA with deafness may be inherited (AR - H+-ATPase)
Kussmaul breathing if severe

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16
Q

Management of RTA

A 
Classic distal (T1)
Sodium alkali or potassium alkali (1mmol/kg) e.g. Shohl’s solution ± potassium supplementation

Proximal (T2 and Fanconi)
Sodium alkali or potassium alkali (1mmol/kg) ± potassium supplementation ± thiazide diuretic

Hyperkalaemia + mineralocorticoid deficiency
Fludrocortisone + dietary restriction of potassium

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17
Q

Complications of RTA (5)

A

Volume depletion - loss of sodium etc at proximal tubule dysfunction
Nephrocalcinosis - classic distal, increased loads of filtered calcium because of release of calc phos and calc carb in bone buffering of acidosis
Osteoporosis - bone buffering of acidosis leads to demineralisation
Growth retardation - acidosis associated with muscle catabolism
Renal rickets - Fanconi, can’t reabsorb phosphate

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18
Q

Causes of end stage renal failure (4)

A

Glomerulonephritis
Pyelonephritis
Diabetes
PKD

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19
Q

Pyelonephritis
What
Bacteria
Risk factors (4)

A

Infection/inflammatory disease of renal parenchyma, calyces and pelvis that may be acute, recurrent or chronic

Gram -ve: E. coli (60%), proteus (15%), klebsiella (15%)
@Diabetes = klebsiella or candida
@HIV, malignancy, transplant = candida

Age - Infants and older
Anatomical abnormality - VUR, PKD, horseshoe, double ureter
Foreign body - Stone, catheter
Impaired renal function
Immunocompromised
Obstruction - BPH, stone, foreign body, bladder neck obstruction, posterior ureteral valve, neurogenic bladder
Pregnant

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20
Q

Pyelonephritis presentation
Tirad
Extras

A

Loin pain
Fever - may not be the case if patient is on steroids or anti-inflammatory
Renal tenderness/costovertebral angle

+ nausea/vomiting, DUF (associated with cystitis or urethritis), rigors

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21
Q

Pyelonephritis Ix (6)

A

URINE MC&S
-Urine dip: blood, protein, nitrites, leukocyte esterase
-Urinalysis
-Gram stain: G -ve rods (e.coli, klebsiella, proteus)
-Urine culture
FBC: leukocytosis
ESR/CRP raised
Blood culture (systemic infection SEPSIS)

IMAGING (mandatory in recurrent pyelonephritis)
*Renal USS: gross abnormality, hydronephrosis, stones, abscess
*Contrast CT: altered perfusion, structural abnormality
DMSA (renal scarring)

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22
Q

Pyelonephritis Mx
Mild
Severe/complicated/pregnant

A

Mild/moderate + uncomplicated
Ciprofloxacin (500mg PO BD 7-14D) or cefixime (400mg PO OD 14D) - 3rd gen

Severe or complicated or pregnant
Admit to hospital
IV ceftriaxone (3rd gen ceph) OR IV ciprofloxacin OR IV gentamicin (not to preg)
IV fluids
IV paracetamol (pain and fever)
Catheterisation if compromised
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23
Q

Renal cell carcinoma
What
Types
Presentation

A

Renal malignancy arising from renal parenchyma/cortex

80% clear cell/adeno renal carcinoma (renal cortical parenchyma) -> due to cholesterol and glycogen
15% papillary tumor (types 1 and 2)

*Haematuria
*Flank pain
*Abdominal mass - * = classical triad <10% cases
Systemic: weight loss, anorexia, malaise
Left sided varicocele by invasion of left renal vein
Lower limb oedema

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24
Q

RCC risk factors

A

Smoking, obesity, HTN, age, renal transplant and dialysis (15%)
+ve family history x4 risk
-Hippel Lindau (AD): 30% develop RCC -> born with germline loss of one VHL tumour suppressor gene.

25
Q

RCC spread
Direct
Lymphatic
Haem

A

Direct - renal vein
Lymphatic - paraaortic then mediastinal
Haem - bone, liver, lung (cannonball mets + colono)

26
Q

Stuaffers syndrome

A

Presence of a RCC causing:
Cholestasis in absence of liver metastasis (elevated bilirubin, alkaline phosphatase and gamma GT) with elevated PT (coag), thrombocytosis and hepatosplenomegaly

27
Q

RCC Ix (5)

A

BP - increased from renin secretion
Percutaneous renal biopsy
FBC - polycythaemia (EPO)
LDH - raised is poor prognosis (x 1.5)
Corrected calcium - >2.5 mmol/l poor prognosis
LFT - raised AST/ALT = metastatic disease
Cr - elevated with reduced clearance
Urinalysis - haematuria and/or proteinuria

*Abdominal/pelvis USS - cyst, mass, mets
*CT abdo/pelvis - lymphadenopathy, mass, bone mets inc contralateral kidney
MRI - for local invasion etc
CXR - cannonball metastasis, bone scan, MRI brain/spine

28
Q

Wilms tumour

A

Nephroblastoma
Childhood tumour of primitive renal tubules and mesenchymal cells
Abdominal mass and haematuria

29
Q

AKI
What
Risk factors

A

Abrupt (within 48 hours)/ absolute increase in:

  • serum creatinine of ≥ 26.4 μmol/l above baseline,
  • a serum creatinine increase of ≥ 50%, or
  • oliguria of less than 0.5 mL/kg per hour for more than six hours

Elderly, DM, dehydration, underlying kidney disease, nephrotoxins & sodium retaining states (CHF, cirrhosis, nephrotic syndrome)

30
Q

Types of AKI (3)

A

Pre-renal (50%)
Azotaemia (high nitrogen compounds e.g. Ur, Cr) due to reduced perfusion causing hypovolaemia, haemorrhage, sepsis, third spacing of fluids (severe panc), overdiuresis, heart failure
Hepatorenal syndrome = azotaemia not responsive to fluids (liver disease)
Renovascular disease - *giving NSAIDs to patient with bilateral renal artery stenosis

Intrinsic (30%)
*Acute tubular necrosis (mainly due to sepsis = most common)
*Rapidly progressive glomerulonephritis
*Interstitial nephritis
Vascular disease: HUS, TTP, scleroderma, atheromatous embolisation, thrombosis

Post-renal (20%)
Mechanical obstruction to urinary tract
Retroperitoneal fibrosis, lymphoma, tumour, prostate hyperplasia, renal calculi, urinary retention, pyelonephritis

31
Q

Acute tubular necrosis

A

Death of tubular epithelial cells that form the renal tubules of the kidneys.

ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI.

Common causes of ATN include low blood pressure and use of nephrotoxic drugs.

32
Q

Nephrotoxic drugs
Prerenal
Intrarenal
Post renal

A

Drugs causing GI loss
NSAIDS -> hypoperfusion
ACEI if compromised renal perfusion (e.g. renal artery stenosis) (DO NOT PRESCRIBE WITH NSAID)

Glomerulonephritis - captopril, penicillamine, gold, penicillins, rifampicin
Interstitial nephritis - penicillins, cephalosporins, thiazide, furosemide, NSAID, rifampicin
ATN - aminoglycosides, amphotericin, ciclosporin

Anticholinergics (TCA) + alcohol -> retention

33
Q

AKI presentation

A

Decreased urine
Vomiting (early could be causative, late could be uraemia)
Dizziness (orthostatic suggests pre-renal)
Orthopnoea (fluid overload)
Altered mental status (uraemia)
Signs of uraemia - asterixis (flapping tremor)
Peripheral oedema
Muscle tenderness (rhabdomyolysis)

34
Q

AKI Ix (6)

A

U+E+Cr: Elevated creatinine, *high serum potassium (or on *VBG), *metabolic acidosis

Urine dip, MC + S - Infection -> leukocytes/nitrates, Glomerular disease -> blood/protein

  • Anaemia (CKD/blood loss), leukocytosis (infx), thrombocytopenia (HUS, TTP)

Imaging *priority if anuric - Renal USS -> obstruction, cysts, mass

ECG - For *hyperkalaemia - increased PR, widened QRS, peaked T, sine wave

Ratio serum urea:creatinine + other tests of cause
20:1 -> pre-renal cause

35
Q

AKI management

A

Stop nephrotoxic drugs
ABCDE
Including fluid challenge if hypotensive, diuretic if hypertensive
Catheterise for accurate urine output
Urgent VBG/ABG (for K+) + ECG
Urgent USS KUB for obstruction (? nephrostomy)
Urine dip for GN/infx
If uraemic, severe metabolic acidosis, severe hyperkalaemia -> dialysis

36
Q

CKD

What

A

Proteinuria or haematuria (evidence of kidney damage) and/or reduction in GFR to <60ml/min/1.73m2 for more than 3 months

37
Q

CKD stages

A

Stage 1: kidney damage with normal or increased GFR (> 90)
Stage 2: kidney damage with mild decrease GFR (60-89)
CKD below
*Stage 3a: kidney damage with mod decrease GFR (45-59)
*Stage 3b: kidney damage with mod decrease GFR (30-44)
*Stage 4: kidney damage with severe decrease GFR (15-29)
*Stage 5: kidney failure (ESRD) with GFR < 15

38
Q

Causes of CKD

A

Diabetes (40% of ESRF): diabetic nephropathy = macroalbuminuria ± reduction in GFR to <90

HTN (33% of ESRF) + renal vascular disease (stenosis)

Glomerular nephrotic/nephritic syndromes:
Focal segmental glomerulosclerosis
Membranous nephropathy
Lupus nephritis
Amyloidosis

Polycystic kidney disease

Obstructive uropathy
Myeloma (due to stones from hypercalaemia)
Renal tumour
BPH
Stones
39
Q

Uraemic syndrome
Symptoms
Complications
Management

A

Fatigue, metallic taste, nausea/vomiting, itch, delirium, seizures, anorexia

Uraemic tinge (grey/yellow)

  • Uraemic encephalopathy
  • Pericarditis
  • Bleeding

Rapid RRT

40
Q

CKD complications (5)

A

Anaemia - due to diminished EPO at S3 signs of anaemia
Renal osteodystrophy - due to elevation in PTH as a result of phosphorus retention and hypocalcaemia from
1,25 vitamin D deficiency as GFR declines phosphate itch, parasthesia, tetany and bone pain, can cause Ca to deposit in blood vessels
CV disease - (CKD is risk factor independent of DM, HTN, dyslipidaemia)
Protein malnutrition - protein loss in urine
Metabolic acidosis - unable to excrete acid at GFR < 50
Hyperkalaemia - unable to excrete potassium as GFR declines
Pulmonary oedema - fluid overload (Rx with loop diuretics)

41
Q

CKD Ix (5)

A

Serum creatinine elevated
Urinalysis: haematuria or proteinuria
Urine microalbumin: microalbuminuria
Renal USS: small kidney, obstruction/hydronephrosis, large kidney (infiltration myeloma, amyloidosis)
eGFR < 60
Blood sugar
FBC - anaemia, normochromic normocytic
Osteodystrophy: hypocalcaemia, hyperphosphataemia and hyperparathyroidism, high alkaline phosphatase
Antibodies: autoantibodies, antibodies to streptococcal antigens of hep B/C antibodies

42
Q

CKD Mx (5)

A

Treat BP + CV risk - ACEI/ARB2 target 140/90 ± 2nd and 3rd line etc…+ Statin, smoking cessation, weight loss, aspirin
Treat anaemia - Epoeitin alfa (EPO stimulating agent) ± ferrous sulfate (oral) if necessary
Treat renal bone disease - Dietary modification (based on Ca and PO4 - milk, cheese, eggs) and phosphate binding drug (calcium acetate/carbonate) ± calcitriol if low
Treat metabolic acidosis - Oral sodium bicarbonate
Treat oedema - Loop diuretics and restrict sodium
High potassium - Low potassium diet

43
Q

Indications for RRT in AKI (6)

A

Uraemia (pericarditis, gastritis, encephalopathy)
Pulmonary oedema (fluid retention) unresponsive med Rx
Severe hyperkalaemia (>6.5) unresponsive to med Rx
Severe hypo/hypernatramia
Severe metabolic acidosis (<7.0) unresponsive to bicarb
Severe renal failure (urea > 30)

44
Q

Renal transplant risks

A

Immediate operative: local infx, pain, DVT
Infections due to immunosuppression (viral HSV for 4 weeks then CMV, bact, fungal)
Urinary tract obstruction
Drug toxicity: bone marrow suppression
*Cancer (skin, lymphoma)
*CV disease (main cause of death), hypertension, dyslipidaemia

Rejection

  • Hyperacute (mins), rare due to crossmatch
  • Accelerated (days), T cell mediated crisis -> fever, swollen kidney, increased Cr -> IV steroids
  • Acute cellular (weeks), 25% in <3 weeks -> fluid retention, rising BP, rising Cr, high dose IV steroids
  • Chronic (years), gradual rise in Cr and proteinuria, resistant HTN -> graft biopsy shows vascular changes, fibrosis and atrophy
45
Q

Glomerulonephritis

A

Glomerular injury by a group of diseases characterised by changes in the glomerular capillaries and glomerular basement membrane. Changes are most likely immune mediated

46
Q

Causes of Glomerulonephritis

A

Commonly idiopathic
Infection - GABH streptococcus (pyogenes), resp/GI infection, hep B/C
Systemic inflammatory conditions - SLE, RA, Goodpasture’s, Wegener’s, HSP, HUS, scleroderma
Drugs - Penicillamine, gold, NSAIDs, ciclosporin, mitomycin
Metabolic - DM, HTN
Malignancy, hereditary, deposition

47
Q

Nephrotic syndrome
Causes (5)
Features

A 
Nephrotic = non-proliferative
Deposition disease (amyloidosis + light chain dep)
Minimal change disease
Focal and segmental GN
Membranous nephropathy
Membranoproliferative GN

Proteinuria (>3.5g/24 hours)
Hypoalbuminaemia (<30g/L)
Peripheral oedema
Hyperlipidaemia

48
Q

Nephritic syndrome
Causes (4)
Features

A 
Nephritic = proliferative
IgA nephropathy (1ary) - Macroscopic haematuria 24/48 hours post GI/URTI &amp; IgA deposition in mesangial matrix

Membranoproliferative - Primary (immune mediated) or secondary (SLE). Thickening of glomerular basement membrane and mesangium

Postinfectious GN (1ary) - Weeks after URTI -> strep pyogenes -> resolves

Rapidly progressive GN

  • Vasculitis - Wegener’s - cANCA & Microscopic polyangiitis - pANCA
  • Anti-GBM GN (1ary) - Goodpasture’s syndrome - AI, antiGBM

Oliguria/AKI (renal dysfunction)
HTN
Haematuria: active urinary sediment (red cells and casts)

49
Q

Nephrotic syndrome complications (5)

A

Susceptibility to infection - increased urinary loss of IgG (streptococcal), or secondary to steroids
Hypercoagubility and thromboembolism - renal vein thrombosis (lupus or urinary loss of antithrombin, altered protein C and S)
Hypercholesterolaemia - increased hepatic lipoprotein synthesis and loss of lipid regulating proteins
Hypervolaemia - severe decrease in GFR resulting in oedema
AKI - more likely with acute GN
HTN - impaired GFR and increased reabsorption of salt and water

50
Q 
Minimal change disease
Who
Cause
Light microscopy &amp; Immunofluorescence
Electron microscopy
Mx
A

Kids - 90% in < 10yrs
Idiopathic, NSAIDs or Hodgkin’s lymphoma
Light microscopy & Immunofluorescence - normal
Electron microscopy - effacement of podocyte foot processes
Responds to steroids

51
Q

Focal segmental glomerulosclerosis
Who
Cause
Light microscopy

A

Younger adults
Idiopathic or secondary to HIV
Light microscopy - segmental areas of mesangial collapse and sclerosis (focal not widespread)

52
Q 
Membranous nephropathy 
Who
Cause
Light microscopy
Immunofluorescence
Electron microscopy
A

Most common adult/older
Usually idiopathic or secondary to Hep B, gold, penicillamine, NSAIDs
Light microscopy - basement membrane thickening and associated cellular proliferation
Immunofluorescence - granular IgG deposition
Electron microscopy - electron dense deposits in subepithelial space

53
Q

Ix for glomerulonephrits
Routine (5)
Specific

A

FBC - anaemia -> systemic
U + E + Cr + LFT -> ?hepatitis, advanced disease, albumin
Urinalysis -> haematuria, proteinuria, RBC casts
GFR -> normal or reduced
Lipid profile + glucose
24 hour urine collection

ESR - vasculitis
Complement - low in immune complex
RF - RA
ANCA - anti GBM disease
Anti GBM antibody - anti-GBM disease or Goodpasture’s
Antistreptolysin O antibody/anti DNase - post strep
Anti DS DNA/ANA - SLE
Hep B/C/HIV serology
Electrophoresis - raised gamma globulin in lymphoma and amyloidosis

54
Q

Glomerulonephritis Mx
Mod - severe (Criteria)
Rapidly progressive (3)

A

(haematuria, proteinuria and reduced GFR)
Oral meds:
Proteinuria reducing meds (ACEI/ARB), + ABX + furosemide + prednisolone (1 mg/kg/day) with immunosuppressant e.g. cyclophosphamide

IV meds:
Anti-GBM - plasma exchange (remove aB) + IV methylprednisolone + IV cyclophos
Immune complex - IV methylpred or oral pred ± ABX
Lupus nephritis - IV methylprednisolone + cyclophosphamide

55
Q

Polycystic kidney disease
Types
Features
Complications

A

2 forms, ADPKD (most common) and ARPKD

Renal cysts, extrarenal cysts (liver), intracranial aneurysms, aortic root dilation and aneurysms, mitral valve prolapse, abdominal wall hernias

HTN, increased CV morbidity, CKD, ruptured intracranial aneurysm, ESRD

56
Q

PCKD presentation

A 
FHx of PKD/ESRD or stroke
Flank/abdominal discomfort due to enlarging kidneys, haemorrhage or stone formation
Lumbar pain (females)
Haematuria (males)
HTN (at 20-35) ****** -> mandatory screening with renal USS
DUFS (infection, UTI)
Palpable kidneys
Headaches (intracranial aneurysm)
Hepatomegaly (liver)
57
Q

PCKD Ix (4)

A

Renal USS -> Ravine’s criteria (With positive fam history)
- <30yrs = 2 or more unilateral or bilateral cysts
- 30-60yrs = 2 cysts in each kidney
- 60+yrs = 4 cysts in each kidney
Genetic testing - PKD1 or PKD2 mutation
CT abdo pelvis
Relevant further testing
Urinalysis (protein, bacteria), ECG - LVH + echo - aortic root dilation, MR angiography - screen for aneurysm

58
Q

PCKD Mx

A

HTN - ACEI or ARB lifelong aim 130/80

UTI/Infected cyst - Ciprofloxacin

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