Renal Flashcards
what is acute kidney injury
- a significant deterioration in renal function
- over hours or days
- 3 stages of severity
what are the three types of causes for AKI
- pre-renal (decreased perfusion to kidney)
- renal (intrinsic renal disease)
- post-renal (obstruction to urine flow)
give 3 pre-renal causes of AKI
- renal artery stenosis
- heart failure
- haemorrhage
give 4 renal causes of AKI
- acute tubular injury
- glomerulonephritis
- acute interstitial nephritis
- renal vasculitis
give 3 post-renal causes of AKI
- benign prostatic hyperplasia
- kidney stones
- tumour
what is the pathology of pre-renal AKI
- low vascular volume
- decreased cardiac output
- systemic vasodilation
- renal vasoconstriction
what is the pathology of renal AKI
- glomerular
- interstitial
- vessels
what is the pathology of post-renal AKI
extrinsic compression
clinical manifestations of AKI
- oliguria (passing small volume of urine)
- severe = pulmonary oedema, encephalopathy, pericarditis
- fatigue
- SOB
- can cause HYPERKALAEMIA = medical emergency
differential diagnoses of AKI
- CKD
- hyperkalaemia/hypernatremia
- acute tubular necrosis
investigations for AKI
- bloods = elevated serum urea and creatinine
- imaging
diagnostic markers for AKI
- rise in creatinine>26umol/L in 48h
- rise in creatinine >50%
- urine output <0.5ml/kg for >6 consecutive hours
management of AKI
- dialysis may be needed while renal function improves
- manage complications (hyperkalaemia, pulmonary oedema, uraemia, acidaemia)
- IV fluid for hypovolaemia (crystalloid to increase intra-vascular volume)
- oxygen, fluid restriction +/- diuretics for hypervolemia
what is chronic renal failure (chronic kidney disease)
- abnormalities of the kidney structure or function with implications for health
- present for >3months
- irreversible loss of nephrons
how is CKD classifies
- based on the cause, GFR category and presence of albuminuria
- GFR<15 is kidney disease
abnormalities of kidney functions/structure
- decreases GFR
- increased albuminuria
- urinary sediment
- electrolyte and other abnormalities
causes of CKD
- acute renal failure
- hypertension
- diabetes
- kidney disease (polycystic kidney disease, dysplastic kidneys, reflux or obstructive nephropathy)
- infections
- drugs
- systemic disease
pathology of CKD
- primary injury to glomeruli, vessels or the tubulo-interstitium
- leads to reduction in nephron mass
- haemodynamic stress on remaining nephrons causes further loss.
clinical manifestations of CKD
- early can be asymptomatic
- tired
- bony pain (decalcification due to metabolic acidosis)
- loss of appetite
- end-stage = fluid overload and metabolic derangement
differential diagnoses for CKD
- AKI
- diabetic nephropathy
- chronic glomerulonephritis
investigations for CKD
- bloods = U&E, Hb, glucose, low calcium, high phosphate, increased PTH
- urine dipstick = albumin:creatinine ratio, protein:creatinine ratio
- US
management of CKD to slow disease progression
- lower BP
- ACE inhibitor
treatment of complications of CKD
- treat anaemia
- sodium bicarbonate supplements if acidosis
- restrict fluid and Na for oedema
- vit D for bone mineral density
- atorvastatin and antiplatelets to prevent CVD and atherosclerosis
renal replacement therapy
- dialysis
- transplant
- preparation should begin when risk of renal failure is 10-20% in a year
complications of CKD
- CVD from hypertension, vascular calcification, hyperlipidaemia
- renal bone disease = mix of hyper-parathyroid bone disease, osteomalatia and osteoporosis
what is haemodialysis
- blood passed over a semi-permeable membrane against the flow of dialysis fluid
- hydrostatic gradient
- AV fistula
- 3+ times per week
what is peritoneal dialysis
- uses the peritoneum as a semi-permeable membrane
- catheter into peritoneal cavity and fluid infused (with osmotic agents)
- drainage
- at home
what is hemofiltration
- water cleared by positive pressure
- low haemodynamic stability so only used in critical care when BP too low for HD
what is glomerulonephritis
-inflammation and damage to the glomeruli which allows protein +/- blood into the urine
what is the condition that causes glomerulonephritis that doesn’t lead to kidney failure
- minimal change disease
pathology of glomerulonephritis
- damage to glomerulus with leakage of proteins and blood
- may be rupture of glomerular basement membrane and a cellular reaction in the Bowman’s space
what are the different types of GN and how do they cause damage to the glomerulus
- immune complex GN and monoclonal immunoglobulin GN = deposition of immune complexes causes local cellular proliferation and inflammation.
- pauci-immune GN = glomerular necrosis.
- anti-GBM GN = Abs against the GBM
- C3 glomerulopathy = abnormalities in the regulation of alternative complement activation with deposition of C3 in the glomerulus
what does GN cause
- haematuria and proteinuria
- damage to glomerulus restricts blood flow; leading to compensatory hypertension
- loss of filtration capacity leads to AKI
clinical manifestations of GN
- asymptomatic urine abnormalities (haem/proteinuria)
- acute nephritis syndrome
- nephrotic syndrome
- CKD
investigations for GN
- assess cause and damage
- bloods: FBC, U&E, LFT, CRP, ANCA, culture, hapatitis serology
- urine: MC&S, bence jones protein, RBC casts
- imaging: CXR (pulmonary haemorrhage), renal US
- renal biopsy required for diagnosis.
what is acute nephritic syndrome
- GN
- immune response triggered by an infection or other disease
- podocytes develop large pores allowing blood and protein into urine.
- red cell casts = distinguishing feature = formed in nephrons and indicate glomerular damage
what is the most common primary cause of acute nephritic syndrome
- IgA nephropathy
what are the symptoms of acute nephritic syndrome
- haematuria
- proteinuria
- hypertension
- oedema
- low vol of urine <300ml/day
what is IgA nephropathy
- immune complex GN related to glomerular deposition of immune complexes containing IgA
causes of IgA nephropathy
- primary = abnormal mucosal immune system produces abnormally glycosylated IgA
- secondary = associated with liver disease, bowel disease and dermatitis herpetiformis.
- systemic form with small-vessel vasculitis
what are the pathological features of IgA nephropathy
- IgA causes glomerular changes from mild mesangial hypercellularity only to glomerular hypercellularity.
- crescents seen in most severe cases
presentation of IgA nephropathy
- asymptomatic non-visible haematuria
- episodic haematuria
- hypertension
investigations/ diagnosis of IgA nephropathy
- renal biopsy = IgA deposition in mesangium
treatment of IgA nephropathy
- ACE inhibitors to reduce BP and protein in urine
what is nephrotic syndrome
- proteinuria due to podocyte pathology = leakage from basement membrane
what is the triad of signs for nephrotic syndrome
- proteinuria >3.5g/24hours
- hypoalbuminemia
- oedema due to oncotic pressure decrease from hypoalbuminemia
- severe hyperlipidaemia (liver goes into overdrive from albumin loss which increases risk of blood clots and raises cholesterol)
causes of nephrotic syndrome
- primary renal disease = minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, membranoproliferative GN
- secondary causes = DM, lupus nephritis, myeloma, amyloid, pre-eclampsia
pathophysiology of nephrotic syndrome
podocyte damage leads to proteinuria
what makes up the kidneys filtration barrier
podocytes, GBM, endothelial cells
presentation of nephrotic syndrome
- generalised pitting oedema to ankles, genital and abdominal wall (rapid and severe)
- hypoalbuminemia
- frothy urine
- systemic symptoms
differential diagnoses for nephrotic syndrome
- congestive heart failure (oedema and raised jugular venous pressure)
- cirrhosis (oedema and hypoalbuminenia)
investigations for nephrotic syndrome
- renal biopsy (find cause)
- urine dipstick (high protein)
- serum albumin low
management of nephrotic syndrome
- reduce oedema (fluid and salt restriction, diuretics with loop diuretics)
- treat cause
- ACEi/ARB reduce proteinuria
what are the complications of nephrotic syndrome
- thromboembolism
- infection
- hyperlipidaemia
what is the pathology of minimal change disease
- nephrotic syndrome
- loss of podocyte foot processes, vacuolation, appearance of microvilli in glomerulus
- proteinuria
- doesn’t progress to renal failure
investigations/diagnosis of MCD
- biopsy= electron microscope shows abnormal podocytes
what is the natural history of MCD
relapsing- remitting course
treatment of MCD
- supportive care
- prednisolone (steroid)
- 2nd line = cyclophosphamide or cyclosporine (immunosuppressants)
what is focal segmental glomerulosclerosis (FSGS)
- nephrotic syndrome
- primary (genetic mutations)
- secondary (HIV/ reflux nephropathy)
investigations for FSGS
- specific segments of certain glomeruli develop sclerosed lesions
- Ab tests all negative
treatment for FSGS
- salt and water restriction and diuretics
- antihypertensives
- statins (for hyperlipidaemia)
- transplant
what is membranous glomerulonephritis
- nephrotic syndrome
- slowly progressive
- usually idiopathic but can be from Hep B/ malaria/ penicillamine/SLE
pathology of membranous glomerulonephritis
- immune complex deposition results in complement activation against GBM proteins
investigations for membranous glomerulonephritis
- microscopic analysis = thickened GBM
- immunofluorescence = diffuse uptake of IgG
treatment of membranous glomerulonephritis
- steroids (prednisolone)
what is the prognosis for membranous glomerulonephritis
1/3 have chronic membranous glomerulonephritis
1/3 go into remission
1/3 progress to end-stage renal failure
what is polycystic kidney disease
- inherited disorder
- clusters of cysts develop primarily within kidneys = enlarge and lose function over time
adult (dominant) polycystic kidney disease
- mutation in PKD1 gene on chromosome 16
- defects in function of PKD1 protein leads to cystic change in renal tubules and loss of normal renal tissue.
- kidneys massively enlarged and completely replaced with cysts
extra-renal manifestations of PKD
- liver cysts
- berry aneurysms
presentation of PKD
symptomatic due to size/haemorrhage
- loin pain
- visible haematuria
- cyst infection
- renal calculi
- hypertension
- progressive renal failure
investigations for PKD
- US
- genetic testing
- CT for renal colic
treatment for PKD
- 3-4 L/day water may supress growth
- high BP treated to target <130/80mmHg (ACEi/ ARB first line)
- treat infections
- cyst decompression for severe/ persistent pain
infantile (recessive) PKD
- rare
- causes bilateral polycystic kidneys with congenital hepatic fibrosis
- mutations in the PKHD1 on chromosome 6p which encodes a component of the cilia on collecting duct epithelial cells
- kidneys enlarged and numerous cysts
- severe cases cause neonatal death from pulmonary hypoplasia
- less severe cause congenital hepatic fibrosis and portal hypertension
- poor prognosis if respiratory distress
treatment for infantile PKD
- continuous renal replacement therapy
what is renal colic
- a type of pain when urinary stones block part of your urinary tract
- upper urinary tract obstruction
what are the symptoms of renal colic pain
- rapid onset
- excruciating ureteric spasms
- pain is from loin to groin
- nausea and vomiting
- worse with fluid loading
- radiates to ipsilateral testis/labia
- can’t lie still
