Renal Flashcards

1
Q

Adrenal cortex mnemonic?

A

GFR-ACD

  • Zona Glomerulosa (outside) - mineralocorticoids (mainly Aldosterone)
  • Zona Fasciculata (middle): glucocorticoids, mainly Cortisol
  • Zona Reticularis (on inside): androgens, mainly Dehydroepiandrosterone (DHEA)
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2
Q

Summary of RAAS?

A
  1. Renin
    • Released by JGA cells in kidney in response to reduced renal perfusion, low sodium
    • Hydrolyses angiotensin to form angiotensin I
    • Stimulated by - low BP/low renal perfusion, hyponatraemia, sympathetic nerve stimulation, catecholamines, erect posture
    • Reduced by - B-blockers, NSAIDs
  2. Angiotensin
    • ACE (lung) converts angiotensin I to angiotensin II
    • Vasoconstriction –> increased BP
    • Stimulates thirst and stimulates aldosterone/ADH release
  3. Aldosterone
    • Released by zona glomerulosa in response to raised angiotensin II, K+ and ACTH levels
    • Causes retention of Na+ in exchange for K+/H+ in distal tubule
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3
Q

Urinalysis patterns?

A
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4
Q

Calcium metabolism?

A
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5
Q

Renal bone disease summary? And clinical manifestations?

A
  • Osteitis fibrosa cystica
    • AKA hyperparathyroid bone disease
  • Adynamic
    • Reduction in cellular activity (both osteoblasts and osteoclasts) in bone
    • May be due to over treatment with vitamin D
  • Osteomalacia
    • Due to low vitamin D
  • Osteosclerosis
  • Osteoporosis
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6
Q

Management of Renal Anaemia?

A
  • Correction of iron with IV if needed
  • Ferritin should be > 200 ng/mL before starting EPO
  • EPO is used to target Hb 10-12 (>11 or hematocrit >33%) reach the target within 4 months
  • Corrected Hb of > 13.5 is associated with HTN crisis
  • Hb < 10.5 increased risk of seizures.
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7
Q

Side effects of EPO?

A
  • HTN and HTN crisis, potentially encephalopathy and seizures (BP increased in 25% of patients)
  • EPO induced seizures occurs after 90 days fro starting the treatment
  • Bone aches
  • Flu-like symptoms
  • Skin rashes, urticaria
  • Pure red cell aplasia* (due to antibodies against erythropoietin)
  • Raised packed cell volume (PCV) = HCT –> increased risk of thrombosis (e.g. Fistula)
  • Iron deficiency 2nd to increased erythropoiesis
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8
Q

Reasons why people fail to respond to EPO?

A
  • Iron deficiency
  • Inadequate dose
  • Concurrent infection/inflammation
  • Hyperparathyroid bone disease
  • Aluminum toxicity
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9
Q

What mediates hyperacute graft rejection?

A

IgG

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10
Q

Graft survival stats?

A

Cadaveric

  • 1 year = 90%
  • 10 years = 60%

Living donor

  • 1 year = 95%
  • 10 years = 70%
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11
Q

Post-op problems for renal transplant?

A

Up to 4 months post-op (can cause graft dysfunction)

  • Acute rejection: risk is great in 1st 2 weeks occurs in 30-50% of cases
  • Ciclosporin toxicity
  • ATN of graft
  • Vascular thrombosis
  • Urine leakage
  • UTI
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12
Q

Management of acute (<6 months) graft failure?

Causes of chronic graft failure (>6 months)?

A

Acute

  • Steroids
  • If resistant use monoclonal antibodies

Chronic

  • Chronic allograft nephrotherapy
  • Ureteric obstruction
  • Recurrence of original renal disease
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13
Q

Autosomal dominant polycystic kidney disease - types, diagnostic criteria?

A

Types

Loci = PKD1 and PKD2 - code for polycystin-1 and 2 respectively

Investigation/Criteria

Abdominal ultrasound

  • Recommended after 20 years of age (risk of false -ve)
  • <30 yrs - 2 cysts, unilateral or bilateral
  • 30-59 yrs - 2 cysts in both kidneys
  • >60 yrs - 4 cysts in both kidneys

Management

  • Analgeisa
  • Abx for UTIs
  • HTN control
  • Transplantation for ESRF
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14
Q

Conditions associated with ADPKD?

A
  • Colonic diverticula
  • Mitral valve prolapse
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15
Q

Autosomal recessive PKD?

A
  • Much less common than ADPKD
  • Chromosome 6
  • Dx - usually on prenatal USS or early infancy with abdo masses and renal failure
  • ESRF in childhood
  • Liver involvement
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16
Q

Nephrotic syndrome causes?

A
  1. Glomerulonephritis (80%)
    • Minimal change GN (75% children)
    • Membranous GN
    • Focal segemnental glomerulosclerosis
  2. Systemic disease
    • Amyloid
    • SLE
  3. Drugs
    • Gold (sodium aurththiomalate), penicillamine
  4. Others
    • Congenital
    • Neoplasia - carcinoma, lymphoma, leukaemia, myeloma
    • Infection - bacterial endocarditis, hep B, malaria
    • Renal vein thrombosis
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17
Q

Complications of nephrotic syndrome

A
  • Infection due to urinary immunoglobulin loss
  • Thromboembolism related to loss of antithrombin III and plasminogen in the urine
  • Hyperlipidemia
  • Hypocalcemia (vitamin D and binding protein lost in urine)
  • Acute renal failure could be due to thrombotic renal veins - loin pain and haematuria.
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18
Q

Types of glomerulonephritis?

A
  1. Membranous GN (Commonest type)
    • Proteinuria/nephrotic syndrome/CRF
    • Cause - infections, rheumatoid drugs, malignancy​, SLE
    • Biopsy - sub-epithelial immune complex deposition (IgG, C3)
    • 1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop CRF
  2. IgA Nephropathy (Commonest worlwide cause of GN)
    • ​Young adult with painless haematuria after UTI
    • Associated with HSP, coeliac, dermatitis herpetiformis
    • Mesangial hypercellularity, +ve immunofluoresence for IgA and C3
    • Good prognosis - frank haematuria
    • Poor prognosis - male, proteinuria, HTN, smoking, high lipids
  3. Diffuse Proliferative GN
    • ​​Post-streptococcal glomerulonephritis in a child
    • Nephritic syndrome/ARF
    • Most common form of renal disease in SLE
  4. Minimal Change Disease
    • ​​Child with nephrotic syndrome
    • Causes - Hodgkin’s, NSAIDs
    • Good response to steroids, next line cyclophosphamide
    • Biopsy - podocyte fusion
    • Rule of 1/3
  5. Focal Segmental GN
    • ​​Idiopathic, or 2ndry to HIV/Heroin, Alport’s, Sickle cell
    • Proteinuria/nephrotic syndrome/CRF
  6. Rapidly Progressive GN (Crescenteric GN)
    • ​​Rapid onset –> ARF
    • Causes - Goodpasture’s, ANCA +ve vasculitis (Wegener’s)
  7. Mesangiocapillary GN (Membranoproliferative)
    • Nephrotic syndrome, haematuria, proteinuria
    • Poor prognosis
    • ​Type 1 - cryoglobulinaemia, hepatitis C –> low C4
    • Type 2 - partial lipodystrophy –> low C3
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19
Q
A
20
Q

Alport’s sydnrome?

A
  • X-linked dominant
  • Defect in gene coding for type IV collagen –> abnormal GBM
  • More severe in males

Presentation

  • Childhood
  • Microscopic haematuria
  • Progressive renal failure
  • Bilateral senorineural deafness
  • Lenticonus - protrusion of lens into anterior chamber
  • Retinitis pigmentosa
21
Q

Alport’s with failing renal transplant?

A
  • Caused by anti-GBM antibodies
  • Leads to Goodpasture’s syndrome picture
22
Q

Risk factors for renal stones? Urate stones? Drug causes?

A

Risk Factors

  • Dehydration
  • Hypercalciuria, hyperparathyroidism, hypercalcemia
  • Cystinuria NOT CYSTINOSIS
  • High dietary oxalate
  • Renal tubular acidosis
  • Medullary sponge kidney, polycystic kidney disease
  • Beryllium or cadmium exposure

Urate stones

  • Gout
  • Ileostomy - loss of bicarb and fluid results in acidic urine –> uric acid

Drug Causes

  • Loop diuretics, steroids, acetazolamide, theophylline –> calcium stones
  • Thiazides can prevent calcium stones (distal tubular calcium resorption)
23
Q
A

Types of Renal Stones?

24
Q

Stag horn calculi?

A
  • Involve the renal pelvis and extend into at least 2 calyces.
  • Develop in alkaline urine and are composed of struvite (ammonium magnesium phosphate, triple phosphate).
  • Ureaplasma urealyticum and Proteus infections predispose to their formation
25
Q

Albumin creatinine ratio?

A

ACR

  • Early morning specimen
  • >2.5 = microalbuminaemia
  • All diabetic patients should be screened annually
26
Q

Management of diabetic nephropathy?

A
  • Dietary protein restriction
  • Tight glycemic control
  • BP control: aim for < 130/80 mmHg
  • Benefits independent of blood pressure control have been demonstrated for ACE inhibitors and angiotensin II receptor blockers - these may be used alone or in combination
  • Control dyslipidemia e.g. Statins
27
Q

CKD stages?

A
  • 1 - >90
  • 2 - 60-90
  • 3a - 45-49
  • 3b - 30-44
  • 4 - 15-29
  • 5 - <15
28
Q

Causes of transient and persistent microscopic haematuria?

A

Transient

  • Urinary tract infection
  • Menstruation
  • Vigorous exercise
  • Sexual intercourse

Persistent

  • Cancer (bladder, renal, prostate)
  • Stones
  • Benign prostatic hyperplasia, Prostatitis.
  • Urethritis e.g. Chlamydia
  • Renal causes: IgA nephropathy, thin basement membrane disease
29
Q

Fanconi syndrome features and causes?

A

Generalized disorder of renal tubular transport resulting in:

  • Type 2 RTA
  • Aminoaciduria
  • Glycosuria
  • Phosphaturia

Causes

  • Cystinosis (most common cause in children)
  • Sjogren’s syndrome
  • Multiple myeloma
  • Nephrotic syndrome
  • Wilson’s disease
30
Q

RTA Types?

A
31
Q

Causes of RTA 4?

A
  • Aldosterone deficiency (hypoaldosteronism): Primary vs. hyporeninemic
  • Aldosterone resistance:
    • Drugs: Amiloride, Spironolactone, Trimethoprim, Pentamidine
    • Pseudohypoaldosteronism
  • DM
32
Q

Cause of RTA 3?

A

Juvenile RTA

Carbonic anhydrase II deficiency

Rarely discussed

33
Q

Differences between ATN and Prerenal Uraemia? (Causes of ARF)

A

Prerenal uraemia = kidneys hold onto sodium to preserve volume

34
Q

Papillary Necrosis - causes and features?

A

Causes

  • Chronic analgesia use
  • Sickle cell disease
  • TB
  • Acute pyelonephritis
  • Diabetes Mellitus

Features

  • Fever, loin pain, haematuria
  • On urogram/pyelogram - papillary necrosis with renal scarring (‘cup and spill’)
35
Q

RCC - location? Associations? Features? Management?

A

Location

  • Most commonly proximal renal tubular epithelium

Associations

  • Middle aged men
  • Smoking
  • Von-hippel-lindau syndrome
  • Tuberous slcerosis

Features

  • Classically - haematuria, loin pain, abdominal mass
  • Pyrexia of unknown origin
  • Left varicocele (occlusion of left testicular vein)
  • Endocrine effects - secretion EPO (polycythaemia), PTH (hypercalcaemia), renin, ACTH

Management

  • Radical nephrectomy
  • a-interferon and IL-2 can reduce tumour size and treat mets
  • Tyrosine kinase inhibitors (nibs)
36
Q

Key features of HIV-associated nephropathy (HIVAN)?

A
  1. Massive proteinuria
  2. Normal or large kidneys
  3. FSGN with focal or global capillary collapse on renal biopsy
  4. Elevated urea and creatinine
  5. Normotension
37
Q

Renal Vascular DIsease - presentation, Ix, Mx?

A

Presentation

  • HTN, CKD, flash pulmonar oedema
  • U+Es worse on ACE

Ix

  • MR angiography/CT angiography

Mx

  • Balloon angioplasty
  • Hypokalaemia and metabolic alkalosis due to compensatory hyperaldosteronism
38
Q

Renal complications of SLE - WHO classification? Management?

A

Classification

  • Class I: normal kidney
  • Class II: mesangial glomerulonephritis
  • Class III: focal (and segmental) proliferative glomerulonephritis
  • Class IV: diffuse proliferative glomerulonephritis
  • Class V: diffuse membranous glomerulonephritis
  • Class VI: sclerosing glomerulonephritis

Management

  • Treat HTN
  • Steroids
  • Immunosuppressants - azathioprine/cyclophosphamide
39
Q

Goodpasture’s - cause? Features? Investigations? Management?

A

Cause

  • Type II hypersensitvity reaction
  • Anti GBM antibodies against type IV collagen
  • Goodpasture antigen - found in kidney and lungs

Features

  • Bimodal distribution, HLA DR2
  • Pulmonary haemorrhage, rapidly progressive glomerulonephritis
  • Factors increasing likelihood of pulmonary haemorrhage - young male, smoking, LRTI, pulmonary oedema

Investigations

  • Renal biopsy - linear IgG deposits along basement membrane
  • Increased TCLO
  • Lung biopsy - accumulation of hemosidren laden macrophages within alveoli

Management

  • Plasma exchange
  • Steroids
  • Cyclophosphamide
40
Q

Haemolytic uraemic syndrome: triad? causes? Ix? Mx?

A

Triad

  • Acute renal failure
  • Migroangiopathic haemolytic anaemia
  • Thrombocytopenia

Causes

  • Post-dysentery - E coli 0157:H7
  • Tumours, pregnancy, cyclosporine, COCP, SLE, HIV

Ix

  • FBC - anaemia, thrombocytopenia, fragmented blood film
  • U+E - renal failure
  • Stool culture

Mx

  • Supportive management
  • No abx
  • Plasma exchange in severe cases with no diarrhoea
41
Q

Phenylketonuria?

A

General

  • Autosomal recessive
  • Defect in phenylalanine hydroxylase - converts phenylalanine to tyrosine –> high levels of phenylalanine –> LD and seizures
  • Chromosome 12

Features

  • Developmental delay
  • Fair hair, blue eyes
  • LD, seizures, eczema
  • Musty odour to urine and sweat

Diagnosis

  • Guthrie test
  • Hyperphenylalaninaemia
  • Phenylpyruvic acid in urine

Mx

  • Dietary restrictions in pregnancy. Poor evidence to suggest strict diet prevents LD.
42
Q

Cystinuria?

A

General

  • Autosomal recessive
  • Formation of recurrent renal stones
  • Defect in membrane transport of COLA (cystine, ornithine, lysine, arginine)

Features

  • Recurrent renal stones - yellow and crystaline - semi-opaque on X ray

Dx

  • Cyanide-nitroprusside test

Mx

  • Hydration
  • D-penicillamine
  • Urinary alkalinization
43
Q

Homocystinuria?

A

General

  • Autosomal recessive
  • Deficiency of cystathione b-synthase –> accumulation of homocysteine

Features

  • Fine, fair hair
  • MSK - similar to Marfan’s - arachnodactyly
  • Neuro - LD, seizures
  • Ocular - downwards discolouration of lens (opposite to Marfan’s)
  • Increased risk of arterial/venous thrombosis (not coronary)
  • Malar flush, levido reticularis

Dx

  • Cyanide nitroprusside test

Mx

  • B6 supplements
44
Q

Alkaptonuria?

A

General

  • Autosomal recessive
  • Phenylalanine and tyrosine metabolism disorder
  • Defect in homogentisate 1,2-dioxygenase. Buildup of tyrosine byproduct (alkapton) accumulates, excreted in urine in large amounts –> cartilage damage, valvular issues, kidney stones
  • Common in Slovakia and Dominican republic

Features

  • Pigmented sclera, darkened skin in sun-exposed areas and around sweat glands
  • Low back pain, hip/shoulder pain –> joint replacement
  • Calcification of and regurg in aortic and mitral valves –> replacement or CHD
  • Ear wax exposed to air turns black or red after several hours

Tx

  • Nitisinone - suppressed homogentisic acid production
45
Q

Adverse effects of BPH treatment?

A

Alpha Blockers

  • Dizziness, postural hypotension
  • Dry mouth
  • Depression

5 alpha-Reductase Inhibitors

(Block conversion of testosterone to DHT)

  • Erectile dysfunction
  • Reduced libido, ejaculation problems
  • Gynaecomastia
46
Q

Prostate Ca Mx?

A

Localised Disease (T1/T2)

  • If life expectancy <10 years - watchful waiting
  • If life expectancy >10 years - radical prostatectomy and radical radiotherapy

Locally Advanced Disease (T3/T4)

  • Beyond prostatic capsule or involving bladder neck or rectum
  • Radiotherapy

Disseminated Disease

  • Synthetic GnRH agonist (Goserelin AKA Zoladex)
    • Provides negative feedback to anterior pituitary
    • Cover with anti-androgen to prevent rise in testosterone
  • Anti-androgen (Cyporterone acetate)
    • ​Prevents DHT binding from intracytoplasmic protein complexes
  • Orchidectomy
47
Q

Risk factors for bladder Ca?

A
  • Smoking
  • Occupational - aniline dyes used in printing/textiles/rubber industry
  • Aromatic amines
  • Radiation treatment to pelvis
  • Schistosomiasis (S.hematobium infection)
  • Mutations (17p13.1 –> p53)
  • Cyclophosphamide