Week 14 - Renal Flashcards
What are some of the functions of the kidney?
Metabolic waste excretion Endocrine functions Drug metabolism/excretion Control of solutes and fluid status Blood pressure control Acid/base balance
What would be a normal amount of protein in the urine?
Less than 150mg of protein / 24h
How would you measure urinary protein excretion?
24 hour urine collection: grams of protein/24hours (this is hard in clinical practice.)
So would normally do:
Protein:creatinine ratio (PCR) on morning spot sample(mg/mmol)
How would you calculate the eGFR?
(urine creatinine concentration x urine volume)/plasma creatine concentration
What GFR would be considered normal unless they had evidence of kidney disease?
≥60 ml/min/1.73m^2
What is glomerulonephritis?
An inflammatory disease involving the glomerulus and the tubules.
What are the three layers of the glomerular filtration barrier?
Endothelial cell Basement membrane Epithelial cells (podocytes)
What are the 4 targets for injury in glomerulonephritis?
Podocytes, glomerular capilliaries, basement membrane, mesangial cells.
How is glomerulonephritis diagnosed?
Kidney cortex biopsy
What are the 3 features of nephrotic syndrome?
- Proteinuria - either 3.5g proteinuria/24 hours or PCR>300
- low serum albumin (<30)
- Oedema
What are the potential complications of nephrotic syndrome?
Risk of venous thromboembolism
Increased risk of infection
What are some secondary causes of glomerulonephritis?
Diabetes Drugs i.e. NSAIDs, bisphosphonates Rheum - RA, lupus, amyloid CV - Subacute bacterial endocarditis Respiratory - bronchiectasis, lung cancer, TB Hepatitis, HIV
Which types of glomerulonephritis would fall under a more nephritic, nephrotic or rapidly progressive glomerulonephritis?
Rapidly progressive - IgA, lupus, vasculitis
Nephritic - IgA, lupus, post-infectious.
Nephrotic - minimal change, FSGS, membranous.
What is the pathology behind IgA nephropathy? How does the clinical picture progress? How is it treated?
IgA depositions in the mesangial cells. 1. haematuria 2. hypertension 3. proteinuria 4. renal failure ACEi, ARBs then corticosteroids if still proteinuria
How does membranous glomerulonephropathy present? What is it often secondary to? What antibodies are present in 70%?
Nephrotic syndrome
Malignancy, CTD, drugs.
Anti-phospholipiase A2 receptor antibody.
How is membranous nephropathy treated?
Treat underlying disease
supportive non-immunological - ACEi, diuretics, statins
Specific immunotherapy i.e steroids, cyclosporin, rituximab, alkylating agents
What age group is minimal change disease most common in? How does it present? What is the pathogenesis? What is it sometimes secondary to?
Children - 90% under 10
Nephrotic syndrome
T cell, cytokine mediated disease targeting the glomerular epithelial cell basement membrane.
URTI, malignancy.
What is the treatment of minimal change disease?
High dose steroids - prednisolone.
What are 3 causes of rapidly progressive glomerulonephritis?
ANCA vasculitis
Goodpasture’s syndrome
Lupus nephritis.
What is the hallmark of diabetic nephropathy? What other diabetic complication is it usually associated with?
Proteinuria
Retinopathy
What is the pathophysiology of diabetic nephropathy?
hyperglycaemia which leads to volume expansion which causes intraglomerular hypertension. This leads to hyperfiltration resulting in protein leaking through into the urine and ultimately, hypertension and renal failure.
How do you prevent people developing diabetic nephropathy?
Tight glycaemic control, control blood pressure well with ACEi, ARBs and SGLT2 inhibitors.
What is the pathogenesis of renovascular disease?
Progressive narrowing of renal arteries with atheroma.
Perfusion is reduced to 20%, GFR falls but tissue oxygenation maintained.
RA stenosis progresses to 70% and cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative processes.
Parenchymal inflammation and fibrosis progress and become irreversible, restoration of blood flow provides no benefit.
How is renal artery stenosis managed?
Blood pressure control (not ACEi/ARB)
Glycaemic control if diabetic.
Smoking cessation, exercise, low sodium diet.
Angioplasty if rapidly deteriorating renal failure.
What is the pathophysiology of lupus nephritis?
Auto-antibodies produced against dsDNA or nucleosomes.
Form intravascular immune complexes or attach to GBM.
Activate complement (low C4)
Renal damage
What is the treatment of lupus nephritis?
Immunosuppression - steroids, MMF, cyclophosphamide, rituximab.
What is the diagnosis of lupus nephritis?
Autoantibodies and renal biopsy.
What is cystitis? What is its presenting features?
Infection of the bladder. Dysuria (pain passing urine) Frequency Urgency Suprapubic pain Haematuria
What is pyelonephritis? What are its presenting features?
All of the features for cystitis...PLUS Fever >38 degrees Chills/rigors Flank pain Costo-vertebral angle tenderness Nausea and vomiting
What are the risk factors for developing UTI?
Infancy - boys and girls under 1 Abnormal urinary tract - congenital or other. Females Bladder dysfunction/incomplete emptying Foreign body i.e. catheters, stones Diabetes mellitus Renal transplant Immunosuppression
How is urinary tract infection diagnosed?
Urinalysis - positive for leucocyte esterase and nitrite.
Microscopy/flow cytometry to detect pus cells and bacteria.
Urine culture
What are the most common bacteria that causes UTI?
E-coli - 90%
Klebsiella
Proteus (kidney stones)
What should be done in ALL children under three when clinical suspicion of a UTI?
Urine culture
What is the management of UTI in children?
Prompt identification - test urine if infant/child presents with urinary symptoms or unexplained fever >38 degrees.
Begin empirical antibiotics while awaiting culture and sensitivities. Oral antibiotic unless severely ill, vomiting or under 6 months.
What IV and oral antibiotics would be used in UTI?
IV - cefriaxone or gentamicin
Oral - co-amoxiclav, nitrofurantoin, trimethoprin, cephalosporin, quinolone.
What imaging modalities are used when investigating UTI?
Ultrasound
MCUG (micturating cystourethrogram)
Nuclear medicine imaging - DMSA, MAG3 indirect cystogram, MAG3 diuesis renogram.
What is vesico-ureteric reflux (VUR)? What does it predispose you to?
Retrograde passage of urine from the bladder into the upper urinary tract.
Recurrent UTIs
What is the management of VUR?
Antibiotic prophylaxis for high grade VUR (grade III-V) until toilet trained by day.
If this failed (i.e. recurrent febrile UTI, new scarring)
STING procedure
Open ureteric re-implantation
Circumcision
What are some of the causes of bladder outlet obstruction?
Posterior urethral valve
Prostatic hypertrophy
Functional neuropathy
Prune belly syndrome
What is the inheritance pattern of adult polycystic kidney disease?
Autosomal dominant
What two genes commonly cause polycystic kidney disease? What is the result of these mutations?
PKD1
PKD2
Overexpression of polycystins in the renal tubular epithelium forming cysts.
What is the natural history of adult polycystic kidney disease?
Cysts gradually enlarge and kidney volume increases. There is some compensation and then eGFR falls, usually 10 years before kidneys fail.
How is APKD diagnosed?
Ultrasound scan
CT or MRI scan more sensitive.
Genetic test
What are the clincial consequences of APKD?
End stage renal disease Cyst accidents - bleeding, infection, rupture Hypertension Intracranial aneurysms Mitral valve prolapse Aortic incompetence Colonic diverticular disease Liver/pancreas cysts Hernias
What is the management of polycystic kidney disease?
Supportive management
Early detection and management of blood pressure
Treat complications
Manage extra-renal associations
Renal replacement therapy i.e. transplant, dialysis
What can be used to treat APKD?
Tolvaptan - vasopressin V2 receptor antagonist to slow cyst formation.
