Renal Flashcards
What are the functions of the kidney?
- filter or secrete waste substances
- retain albumin + circulating cells
- control BP
- activate 25-hydroxy vitamin D
- synthesises EPO
What is the normal GFR?
120ml/min
What is fanconi syndrome?
A rare condition
Failure of the PCT to absorb
How does fanconi syndrome present?
Polyuria, glycosuria, aminoaciduria, rickets, phophaturia, metabolic acidosis
What can cause fanconi syndrome?
- cystinosis
- tenofovir
- paraprotein disease
- Wilson’s disease
- glycogen storage disorders
- sjorgren’s syndrome
- nephrotic syndrome
What is IgA nephropathy?
aka Bergers disease or mesangioproliferative GN
Abnormality in IgA glycosylation leads to deposition of IgA in the mesangial cells surrounding the glomerular capillaries.
What is the commonest cause of glomerulonephritis worldwide?
IgA nephropathy
What is IgA nephropathy often assoc with?
Tonsillitis
Macroscopic haematuria
What are the common locations for renal stones?
Pelviureteric junction
Pelvic brim
Vesicoureteric junction
RF for renal stones?
Anatomical abnormalities (e.g. obstruction) Family history Chemical composition of urine Dehydration Infection Primary renal disease Gout Diet (high oxalate levels) Drugs (diuretics)
What are some different types of renal stones?
Calcium stones
Uric acid stones
Infection induced stones
Cystine stones
How do renal stones present?
Mostly asymptomatic Renal colic Dysuria Recurrent UTIs Haematuria
Describe renal colic?
Rapid onset Excruciating ureteric spasms Pain is from loin to groin and comes and goes in waves Worse when fluid loading N+V
How are renal stones diagnosed?
1st line: Kidney-Ureter Bladder X-Ray
Gold standard: Non-contrast Computerised Tomography (NCCT-KUB)
Other: USS, bloods, urine dipstick
How are renal stones treated?
IV diclofenac
IV cefuroxime if infection
Antiemetics
If <5mm in lower ureter, 90% pass spontaneously
If >5mm and pain = medical expulsive therapy:
- oral nifedipine
If still not passing:
- Extracorporeal shockwave lithotripsy
- Endoscopy with YAG
- Percutaneous nephrolithotomy
How can you prevent renal stones?
Active lifestyle
Over hydration
Low salt and calcium diet
Allopurinol (prevents uric acid stones)
What is AKI?
An abrupt sustained rise in serum urea and creatinine due to a rapid decline in GFR, leading to failure to maintain fluid, electrolytes and acid-base homeostasis.
What staging system is used to classify AKI?
KDIGO
Criteria:
1. rise in creatinine >26umol/L in 48hours
2. rise in creatinine >1.5 x baseline
3. urine output <0.5mL/kg/h for >6hrs consecutively
Need ONE to diagnose
What are some pre-renal causes of AKI?
Renal hypoperfusion
Hypovolaemia
Low cardiac output
What are some intrinsic renal causes of AKI?
Acute tubular necrosis Glomerular: glomerulonephritis or nephrotic syndrome Drugs Renal parenchyma damage Vascular - renal artery/vein thrombosis - vasculitis - HUS
What are some post renal causes of AKI?
Urinary tract obstruction
Stones, clots
Extrinsic compression (e.g. malignancy)
Strictures (e.g. malignancy)
RF for AKI?
>75years Heart failure Poor fluid intake/increase loss Peripheral vascular disease Sepsis Diabetes Prostate cancer
How does AKI present?
O/E:
- palpable bladder + kidneys
- pelvic masses
- oedema
Oliguira Thirst Pericarditis SOB Postural hypotension High urea Sx
What are symptoms of high urea levels?
Fatigue, weakness, anorexia, N+V, confusion, seizures, coma, pruritus, bruising
How is AKI diagnosed?
Serum calcium, phosphate and uric acid Urine disptick Blood count (v high ESR) USS (obstruction) ECG CXR (pul oedema) CTKUB Renal biopsy
How is AKI treated?
Pre-renal: correct volume depletion with fluids, treat sepsis with Abx
Intrinsic renal: refer to nephrology
Post renal: catheterise, CTKUB, cystoscopy + retrograde stents
> sodium bicarbonate for acidosis > diuretics for pul oedema > optimise fluid balance > stop nephrotoxic drugs > consider dialysis
What is the most common cause of AKI?
Acute tubular necrosis
What is acute tubular necrosis?
Necrosis of renal tubular epithelial cells severely affects the functioning of the kidney. It is reversible in the early stages if the cause is removed.
What can cause acute tubular necrosis?
Renal ischaemia
- shock, sepsis, decreased renal perfusion
Toxins
- ahminoglycosides, tumour lysis syndrome, myoglobin secondary to rhabdomyolysis, contrast agents, urinary cast proteins
What are the phases of acute tubular necrosis?
Oliguric - Polyuric - Recovery
What are the features of acute tubular necrosis?
Raised: urea, creatinine, potassium
Muddy brown casts in urine
What is seen on histology for acute tubular necrosis?
Tubular epithelium necrosis
- no nuclei, eosinophilic homogenous cytoplasm
Dilation of tubules
Necrotic cells obstruct tubule lumen
What is glomerulonephritis?
Group of parenchymal kidney diseases that all result in inflammation of the glomeruli and nephrons:
- acute nephritic syndrome
- nephrotic syndrome
- asymptomatic urinary abnormalities
- CKD
What is acute nephritic syndrome?
Often caused by an immune response triggered by infection of other disease. Characterised by:
- haematuria
- proteinuria
- HTN
- oedema
What is the commonest cause of acute nephritic syndrome?
IgA nephropathy
What can cause acute nephritic syndrome?
Post-strep infection SLE IgA nephropahty Infective endocarditis Good pastures disease Systemic sclerosis ANCA-assoc vasculitis Malaria, schistomiasis, hep B+ C Bacterial infection (e.g. MRSA)
What is good pastures disease?
Type 2 hypersensitivity reaction
Co-existance of acute glomerulonephritis and pulmonary alveolar haemorrhage and circulation antibodies directed against an intrinsic antigen to BM of kidney and lung.
Tx: plasma exchange
How does acute nephritic syndrome present?
Haematuria Proteinuria Hypertension + oedema Oliguira Uraemia
How is acute nephritic syndrome diagnosed?
Measure eGFR, urine analysis
Culture throat swabs
Renal biopsy if necesary
How is acute nephritic syndrome treated?
Depends on what causes it
Treat HTN with salt restriction, loop diuretics and CCB
What is the triad in nephrotic syndrome?
- proteinuria >3.5g/24hrs
- hypoalbuminaemia
- oedema
What can cause nephrotic syndrome?
Primary causes:
- minimal change disease
- membranous neuropathy
- focal segmental glomerulosclerosis
Secondary causes:
- diabetes
- amyloid
- infections
- SLE, RA
- drugs
- malignancy
How does nephrotic syndrome present?
Frothy urine
Pitting oedema of ankles, genitals, abdominal wall + face
Proteinuria
Hypoalbuminaemia
How is nephrotic syndrome diagnosed?
Renal biopsy
Urine dipstick
CXR or USS
Antiphosplipase A2 receptor antibody
Complications of nephrotic syndrome?
Susceptibility to infection
Thromboembolism
Hyperlipidaemia
How is nephrotic syndrome treated?
Reduce oedema: diuretics
Reduce proteinuria: ACE-i, ARB
Reduce risk of compilations: anticoagulants, statins
What is minimal change disease?
Disease of kidney that can cause nephrotic syndrome. Mainly in boys under age of 5.
How does minimal change disease present?
- proteinuria
- oedema (mainly face)
- fatigue
- frothy urine
What is seen on electron microscopy in minimal change disease?
Fusion of food processes of podocytes
> diagnosed on biopsy
How is minimal change disease treated?
High dose corticosteroids (e.g. prednisolone)
Relapse: cyclophosphamide or ciclosporin
What can cause asymptomatic urinary abnormalities?
IgA nephropathy
Thin membrane disease
What is CKD?
Longstanding, usually progressive, impairment in renal function for >3months.
GFR<60ml/min/1.73m^2 for >3months with or without evidence of kidney damage.
What can cause CKD?
T2DM HTN PCKD Amyloidosis FHx
How does CKD present?
Asymptomatic in early stages Itching Anorexia + weight loss Nocturia + polyuria Peripheral or pulmonary oedema N,V,diarrhoea
Complications of CKD?
Anaemia Bone disease Postural hypotension CVD Pruritus
How is CKD diagnosed?
Urinalysis: haematuria, proteinuria Urine microscopy: WCC, eosinophilia High urea + creatinine, high alk phosphatase Biopsy + histology Imaging
How is CKD treated?
Treat underling cause of renal disease and limit progression of complications
What is third space?
Where fluid doesn’t normally collect in large amounts
- pul oedema + pleural effusion
- ascites
- bowel obstruction
- intra-abdominal collection/bleed
What is euvolaemia?
No signs or symptoms of hypo or hypervolaemia
How do you manage hypovolaemia?
Oral fluid if able
IV fluid if very ill
How do you manage hypervolaemia?
Diuretics (oral or IV)
Fluid restriction
What are the types of IV fluid?
Crystalloid
Colloid
Explain crystalloid fluid
Small molecules which pass through cell membrane. Move from intravascular space to extravascular space.
Salt containing fluid stays in intravascular space a bit longer than 5% dex.
e.g. Isotonic solutions:
5% dextrose, 0.9% NaCl, Hartmann’s solution
Explain colloid fluid
Large molecules which do not pass through cell membrane. Remains in intravascular compartment. Also expand intravascular volume through higher oncotic pressure.
e.g. gelofusine (contains modified fluid gelatine)
What is renal cystic disease?
Solitary or multiple renal cysts
- simple, polycystic, hydronephrosis, acquired cystic disease, medullary sponge, dysplasia
Describe congenital renal cysts?
Present at birth
- uni/bilateral
- isolated to kidney
- autosomal dom/rec
- genetic mutation leads to predisposition for cyst formation
Describe acquire renal cysts?
Develop over time No genetic mutation - bilateral/unilateral - isolated to kidneys - normal/small kidney size - assoc with CKD
What is ADPKD?
Autosomal dominant polycystic kidney disease
Multiple cysts develop, gradually + progressively, throughout the kidney resulting in renal enlargement and kidney tissue destruction.
> commonest inherited kidney disease
high penetrance
What is the mutation in ADPKD?
85%: PKD1 gene on Chr 16
15%: PKD2 gene on Chr 4
How does ADPKD present?
Can be clinically silent for many years Loin pain Haematuria Nocturia Renal stones Bilateral kidney enalrgemtn Renal colic HTN SAH Pancreatitis Ovarian cysts