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Nephrology Flashcards

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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

Study These Flashcards
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
RCC spread Direct Lymphatic Haem
Direct - renal vein Lymphatic - paraaortic then mediastinal Haem - bone, liver, lung (cannonball mets + colono)
26
Stuaffers syndrome
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
RCC Ix (5)
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
Wilms tumour
Nephroblastoma Childhood tumour of primitive renal tubules and mesenchymal cells Abdominal mass and haematuria
29
AKI What Risk factors
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
Types of AKI (3)
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
Acute tubular necrosis
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
Nephrotoxic drugs Prerenal Intrarenal Post renal
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
AKI presentation
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
AKI Ix (6)
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
AKI management
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
CKD | What
Proteinuria or haematuria (evidence of kidney damage) and/or reduction in GFR to <60ml/min/1.73m2 for more than 3 months
37
CKD stages
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
Causes of CKD
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
Uraemic syndrome Symptoms Complications Management
Fatigue, metallic taste, nausea/vomiting, itch, delirium, seizures, anorexia Uraemic tinge (grey/yellow) * Uraemic encephalopathy * Pericarditis * Bleeding Rapid RRT
40
CKD complications (5)
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
CKD Ix (5)
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
CKD Mx (5)
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
Indications for RRT in AKI (6)
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
Renal transplant risks
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
Glomerulonephritis
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
Causes of Glomerulonephritis
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
Nephrotic syndrome Causes (5) Features
``` 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
Nephritic syndrome Causes (4) Features
``` Nephritic = proliferative IgA nephropathy (1ary) - Macroscopic haematuria 24/48 hours post GI/URTI & 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
Nephrotic syndrome complications (5)
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
``` Minimal change disease Who Cause Light microscopy & Immunofluorescence Electron microscopy Mx ```
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
Focal segmental glomerulosclerosis Who Cause Light microscopy
Younger adults Idiopathic or secondary to HIV Light microscopy - segmental areas of mesangial collapse and sclerosis (focal not widespread)
52
``` Membranous nephropathy Who Cause Light microscopy Immunofluorescence Electron microscopy ```
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
Ix for glomerulonephrits Routine (5) Specific
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
Glomerulonephritis Mx Mod - severe (Criteria) Rapidly progressive (3)
(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
Polycystic kidney disease Types Features Complications
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
PCKD presentation
``` 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
PCKD Ix (4)
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
PCKD Mx
HTN - ACEI or ARB lifelong aim 130/80 | UTI/Infected cyst - Ciprofloxacin

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