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Nephrology Flashcards

1
Q

Describe the pathophysiology, presentation and management of renovascular disease

A

Progressive narrowing of the renal arteries with atheroma causes reduced perfusion. GFR falls but tissue oxygenation of the cortex and medulla is maintained

Progression of RA stenosis to 70% causes cortical hypoxia and microvascular damage and activation of inflammatory and oxidative pathways.

Parenchymal inflammation and fibrosis progress and become irreversible and at this point, restoration of blood flow has no benefit

Presents with hypertension, pulmonary oedema, bruits, hx of vascular disease

Manage with BP control (not ACEi/ARB), statins, good glycaemic control if diabetic, smoking cessation, exercise, low sodium diet

Angioplasty only used if rapidly deteriorating renal failure, uncontrolled HTN or flash pulmonary oedema

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2
Q

Define acute kidney injury and describe factors contributing to its development

A

‘decline of renal excretory function over hours or days, recognised by the rise in serum creatinine and drop in urine output’

Pre-Renal - Circulatory Failure/Shock - Reduced Perfusion of the Glomerulus

Renal - Cells of the Kidney

Post-Renal - Obstruction

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3
Q

Define glomerulonephritis

A

Glomerulonephritis (GN) is a renal disease characterised by inflammation and damage to the glomeruli that allows protein (+/- blood) to leak out into the urine

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4
Q

State methods of assessing kidney function and their uses and limitations

A
  • 24hr Urine Collection (g/24h)
    • Cumbersome, not routinely used in clinical practice
  • Protein:Creatinine Ratio (PCR) (mg/mmol)
  • Albumin:Creatinine Ratio (mg/mmol)
  • Estimation of GFR
    • Based on plasma creatinine concentration
    • Not suitable in AKI
    • Affected by muscle mass
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5
Q

Describe the pathophysiology, presentation and management of amyloidosis

A

Deposition of highly stable insoluble protein material in extracellular space in the kidney, heart, liver and gut

AA = Systemic Amyloidosis - Treat underlying source of inflammation/infection

AL = Immunoglobulin fragments from haematological conditions (e.g. myeloma) - Treat the underlying haematological condition

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6
Q

State common types of renal stones

A
  • Calcium (80%)
    • Calcium Oxalate Monohydrate or Dihydrate
    • Calcium Phosphate
  • Infection (10%)
    • Struvite
  • Uric Acid Stone (5%)
    • Not seen on X-Ray
  • Others (1%)
    • Cystine, Xanthine, Silica
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7
Q

State functions of the kidneys

A

Metabolic waste excretion

Endocrine functions

Drug metabolism/excretion

Control of solutes and fluid status

Blood pressure control

Acid/base balance

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8
Q

State indications for renal replacement therapy

A

Hyperkalaemia

Acidosis

Uraemia

Fluid Overload (hypertension, pulmonary oedema)

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9
Q

Describe the management of UTI

A

Treatment with antibiotics empirically while awaiting cultures and sensitivities

Oral therapy should be used unless severely ill, vomiting or in infants <3 months

Oral - Trimethoprim, Cephalosporin, Co-Amoxiclav, Nitrofurantoin

IV - 3rd Gen Cephalosporins (Ceftriaxone) or Aminoglycosides (Gentamicin)

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10
Q

Describe IgA nephropathy, its diagnosis and management

A

Most common type of GN in adults worldwide

Proliferative

Characterised by mesangial proliferation, increased IgA production and IgA deposition

Often presents 24-48hrs after a URTI

Can present with haematuria, hypertension and proteinuria (nephritic syndrome)

Biopsy needed for definitive diagnosis

Managed with anti-hypertensives, ACEi, steroids

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11
Q

Describe the pathophysiology of renal stone disease

A
  • Abnormal Urine
    • Too much calcium
    • Too much acid
    • Hypercalciuria
    • Hyperoxaluria
    • Stone inhibitors (citrate, magnesium)
  • Obstruction
    • Congenital or Acquired
  • Infection
    • Particularly urease-producing organisms
    • Raises urine pH
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12
Q

Describe the two main congenital abnormalities of the kidneys and urinary tract

A
  • Vesico-Ureteric Reflux
    • Retrograde passage of urine from the bladder into the upper urinary tract
    • May present with UTI and pyelonephritis
    • Can result in renal scarring
    • Low-grade VUR is more likely to spontaneously resolve
    • Manage with antibiotic prophylaxis or STING procedure or open ureteric re-implantation surgically
  • Bladder Outlet Obstruction
    • Posterior Urethral Valve
    • Antenatal hydronephrosis, UTI, poor urinary stream, renal dysfunction
    • Manage with valve resection, antibiotic prophylaxis, CKD care
  • Pelvi-Ureteric Junction Obstruction
    • Abdominal mass, pain, haematuria, UTI
    • Manage with pyeloplasty
  • Vesico-Ureteric Junction Obstruction
    • Anatomical or functional narrowing
    • Antenatal dilation, UTI, abdominal mass, pain, haematuria
    • May improve or resolve spontaneously
    • May need resection
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13
Q

Describe the medical management of chronic kidney disease

A
  • Treatment to slow renal disease progression
    • Aggressive BP control (ACEi/ARB)
    • Improved glycaemic control
    • Exercise
    • Sodium restriction
  • Treatment of renal complications
    • Manage anaemia (iron, B12, folate, EPO stimulator)
    • Acidosis (sodium bicarb supplements)
    • Oedema (fluid/sodium restriction, diuretic)
    • Bone mineral disorders (Vit D supplements, phosphate binders)
  • Other
    • Statins
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14
Q

Describe other inherited cystic disorders of the kidneys

A
  • Von Hippel Lindau
    • Autosomal dominant
    • Causes multiple benign and malignant neoplasms
    • Renal cysts and multifocal renal cell carcinomas
  • Tuberous Sclerosis
    • Autosomal dominant
    • Benign hamartomas of multiple systems (brain, eyes, heart, lung, liver, skin, kidney)
    • Up to 80% have renal involvement with multiple cysts, angiomyolipomas (high risk of bleeding) and renal cell carcinoma
    • Replacement of renal tissue leads to kidney failure
  • Medullary Cystic Kidney Disease
    • Autosomal dominant
    • Cysts at the cortico-medullary junction
    • Causes hyperuricaemia and gout
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15
Q

Describe the diagnosis of UTI/Pyelonephritis

A
  • Multistix
    • Useful for children >3 years
    • +ve LE & Nitrite = UTI in 90%
  • Microscopy/Flow Cytometry
    • If -ve for pus cells and bacteria = No UTI
  • Urine Culture
    • Single Organism >= 105 CFU/ml
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16
Q

Define nephrotic syndrome

A

3.5g Proteinuria per 24h (Urine PCR>300)

Serum Albumin <30

Oedema

(Hyperlipidaemia)

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17
Q

Describe minimal change glomerulonephritis

A

Non-proliferative

Most common GN in children

Presents with nephrotic syndrome

Often idiopathic, but can be secondary to malignancy

Electron microscopy shows fused podocyte foot processes

Manage with supportive care (e.g. to reduce oedema) and prednisolone

18
Q

Describe membranous glomerulonephritis, its diagnosis, management and prognosis

A

Presents with nephrotic syndrome

Non-proliferative

Caused by immune complex deposition, which results in complement activation against glomerular basement membrane proteins

Microscopic analysis shows thickened glomerular basement membrane

Immunofluorescence shows diffuse uptake of IgG

Treat underlying disease if secondary

Supportive non-immunological - ACi, statin, diuretics, salt restriction

Immunotherapy can be used if disease progresses (steroids, cyclosporin)

1/3rd spontaneously remit, 1/3rd have chronic membranous GN, the remaining 1/3rd progress to end-stage renal failure

19
Q

Define chronic kidney disease and a system to classify its severity

A

‘kidney damage or GFR <60ml/min per 1/73m2 for three months or more’

Classified based on eGFR

20
Q

Describe haemodialysis and its potential complications

A

Aims to remove solutes (potassium, urea) by diffusion and fluid by convection

Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction

DIffusion of solutes occurs down the concentration gradient

Access is usually through an arteriovenous fistula

Most commonly hospital-based

Standard regimen is 4 hours, 3 times a week

Problems include access complications, hypotension, cramps, fatigue, infection, dialysis disequilibrium

21
Q

State risk factors for UTI

A

Infancy (<1 yr)

Abnormal Urinary Tract (Congenital or Other)

Female Sex

Bladder Dysfunction/Incomplete Emptying

Foreign Body (Catheter, Stone)

Diabetes Mellitus

Renal Transplant

Immunosuppression

22
Q

State the range of organisms that cause UTI

A

Usually anaerobes and gram -ve bacteria from bowel/vagina

E.coli is the most common community organism

Staphylococcus saprophyticus and klebsiella pneumonia are other organisms involved

23
Q

Describe the pathophysiology, presentation and management of diabetic nephropathy

A

Hyperglycaemia leads to volume expansion, intra-glomerular hypertension, hyperfiltration, proteinuria, hypertension and renal failure

Diabetic disease induces structural changes, thickening of glomerular basement membrane, fusion of podocyte foot processes and loss of podocytes

Often presents after retinopathy with proteinuria as a hallmark

Mainstay of treatment is tight glycaemic control, good BP control (with ACEi/ARB) and SGLT-2 inhibitors

24
Q

Describe the pathophysiology, presentation and management of SLE

A

Auto-immune disease with immune complex mediated glomerular disease

Multiple autoAbs, directed against DNA, histones etc.

Form intravascular immune complexes or attach to GBM

Complement is activated leading to renal damage

Can present with elevated creatinine, proteinuria, nephritic syndrome

Treated with immunosuppression - steroids, rituximab, cyclophosphamide

25
Describe peritoneal dialysis and its potential complications
Uses the peritoneal membrane as a semi-permeable membrane Catheter inserted into the peritoneal cavity and fluid is infused Glucose is used as an osmotic agent to achieve ultrafiltration Continuous process, home based Requires patient to drain and refill Complications include peritonitis, infection, hernia, loss of membrane function, glucose load
26
Describe rapidly progressing (cresentic) glomerulonephritis, its diagnosis and management
An aggressive form of GN Progresses to end-stage renal failure over a few weeks if left untreated Common Causes: Goodpasture's - Antibodies against glomerular basement membrane (anti-GBM), present with nephritic syndrome and haemoptysis, require high dose immunosuppression (IV Prednisolone and Cyclophosphamide) Microscopic Polyangiitis - MPO Antibody, +ve pANCA Granulomatosis with Polyangiitis - PR3 Antibody, +ve cANCA
27
Describe the emergency management of acute kidney injury
Protect Airway and Breathing Restore Renal Perfusion Assess for Pulmonary Oedema Treat Hyperkalaemia if \>6.5 (Calcium Chloride, IV Insulin, Salbutamol or Renal Replacement) Treat Sepsis Remove Offending Drugs Correct Acidosis Indications for RRT - Persistent Hyperkalaemia, Acidosis, Uraemia (pericarditis, encephalopathy), Toxins
28
Describe the clinical consequences of progressive chronic kidney disease
Albuminuria Pruritis, Nausea, Anorexia, Weight Loss, Fatigue, Leg Swelling, Breathlessness, Nocturia, Joint/Bone Pain, Confusion Peripheral/Pulmonary Oedema, Pericardial Rub, Rash, Hypertension, Tachypnoea, Cachexia, Pallor
29
Describe post-infectious glomerulonephritis, its diagnosis and management
Proliferative Can occur after almost any infection, particularly after strep. pyogenes Anti-body production and sub-epithelial deposition of immune complexes Presents with oliguria, haematuria, proteinuria, oedema and hypertension May require dialysis or antibiotics Usually resolves over weeks, and almost always a benign prognosis
30
Describe the pathophysiology, presentation and management of renal cancer
Renal cell carcinoma is the most common, others include transitional cell carcinoma, sarcoma and metastases 80% are found incidentally Systemic symptoms include night sweats, fever, fatigue, weight loss, haemoptysis 10% present with the classic triad (mass, pain, haematuria) Initial diagnosis is made with USS, CT, MRI or renal biopsy Manage with partial or radical nephrectomy, cryotherapy
31
Describe the epidemiology of renal stone disease
10-15% Lifetime Risk Peak Incidence of 30-50 Yrs Males \> Females Caucasian\>Asian\>Black\>Hispanic More common in hot, dry climates Risk of further stone is 50% at 10 years and 90% at 30 years
32
Describe adult polycystic kidney disease, its presentation and management
Autosomal dominant Most common inherited kidney disorder Most are associated with PKD-1 gene mutation, some with PKD-2 gene mutation These genes code for Polycystin 1 and 2, located in renal tubular epithelia and overexpressed in cyst cells, membrane proteins involved in intracellular calcium regulation Cysts gradually enlarge, kidney volume increases and there is some compensation eGFR falls, usually 10yrs before the kidney fails Diagnosed with USS: If FHx - Age 15-30, 2 Unilateral or Bilateral Cysts. Age 30-59, 2 Cysts in Each Kidney. \>60, 4 Cysts in Each Kidney If No FHx - 10 or More Cysts in Both Kidneys, Renal Enlargement, Liver Cysts Complications: End stage renal failure, hypertension, hernias, liver/pancreas cysts Management is supportive, BP control, treat complications and extra-renal associations May require renal replacement therapy Tolvaptan - Vasopressin V2 receptor antagonist, can delay onset of RRT by around 4-5yrs. S/E include hepatotoxicity and hypernatraemia
33
Describe the diagnostic process in acute kidney injury
Rise in serum creatinine \>26micromol/L Rise in serum creatinine \>1.5x baseline Urine output \<0.5ml/kg/h for \>6 consecutive hours 1. CKD or AKI? 2. History and Exam (Sepsis, Haemoptysis, Rhabdo) 3. Drugs 4. Urinalysis 5. Renal USS 1. Exclude obstruction 2. Info on kidney size 6. GN Screen 1. ANCE, ANA, Ig, Complement, aGBM, Urine Bence Jones Protein 7. Other Blood Film
34
Describe the presentation of renal stones
Incidental Pain (colic, radiates from loin to groin, cannot settle, unable to stay still) Haematuria UTI Sepsis Investigate with CT, Bloods (U&Es, CRP, FBC), Urinalysis, Urate, Calcium
35
Describe other inherited renal disease
* Alport's Syndrome * Usually X-Linked * Abnormality in Collagen IV (found in basement membranes, so associated with anti-GBM disease) * Presents with haematuria, proteinuria and progressive renal insufficiency * Results in renal failure * Often associated with sensorineural hearing loss * Fabry's Disease * X-Linked * Lysosomal storage disorder due to deficiency of alpha-glucosidase * Causes proteinuria, end-stage renal failure, lipid deposits in urine * Manage with IV enzyme replacement therapy
36
Describe the pathophysiology and clinical presentation of pyelonephritis
UTI refers to infection anywhere along the urinary tract, from kidney to urethra Pyelonephritis specifically refers to infection of the kidney/renal pelvis Presents with dysuria, frequency, urgency, suprapubic pain, haematuria, fever, chills/rigor, flank pain, costovertebral angle tenderness, nausea, vomiting
37
State the aetiology of acute and chronic glomerulonephritis
Group A Strep Systemic Inflammatory Diseases (SLE, RA) Drugs (e.g. NSAIDs) Diabetes Hypertension Amyloidosis
38
Describe the short and long-term consequences of renal transplantation
Far better outcome than dialysis Cadaveric waiting list of approx. 3 years * Pros * No dialysis * Better level of renal function * Can live much more independently * Better life expectancy * Better fertility * Cons * Immunosuppressive medication for duration of transplant * Increased CV risk * Increased infection * Post-transplant diabetes * Skin malignancies and others * Risk of acute/chronic rejection, surgical bleeds Immunosuppression with monoclonal antibodies, calcineurin inhibitors antimetabolites, glucocorticoids
39
Describe the pathophysiology, presentation and management of bladder cancer
Majority are transitional cell carcinomas Can be squamous carcinomas and adenocarcinomas Classically presents with painless frank haematuria Diagnosed with flexible cystoscopy Manage with mitomycin, chemotherapy, radical cystectomy, radiotherapy If metastatic, treat with M-VAC chemotherapy (methotrexate, vinblastine, doxorubicin, cisplatin)
40
Describe the pathophysiology, presentation and management of prostate cancer
Most are primary adenocarcinoma, usually arising in the peripheral zone of the prostate May be asymptomatic or present with painful/slow micturition, UTIs, haematuria, retention, lymphoedema Metastatic features may include bone pain and renal failure due to ureteric obstruction Diagnosed by digital rectal examination, prostate-specific antigen and trans-urethral guided needle biopsy Note that PSA is tissue, not tumour specific and tends to rise with age Manage localised disease with surveillance, radiotherapy, radical prostatectomy, cryotherapy For advanced cancer, androgen ablation therapy (medical or surgical castration), chemotherapy, radiotherapy
41
Describe the pathophysiology, presentation and management of testicular cancer
Most are germ cell tumours (seminoma, teratoma) but can be stromal (leydig or sertoli) or lymphoma Majority present as a painless lump, or may be found after incidental trauma Investigate with scrotal USS, alpha-fetoprotein, Beta-hCG, LDH Treat with radical orchidectomy, chemotherapy, nodal radiotherapy
42
Describe the management of renal stone disease
Analgesia (NSAIDs, e.g. Diclofenac) Small stones are likely to pass spontaneously Larger stones or if non-remitting pain, may require medical expulsive therapy (alpha-blocker - tamsulosin) Surgical options include Extracorporeal Shockwave Lithotripsy, Ureteroscopy with Basket Extraction or Percutaneous Nephrolithotomy

Phase 3 (14 decks)

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