Renal Flashcards
Renal anatomy
Kidneys lie retroperitoneal. L is slightly higher with its haul @ L1 due to the presence of the liver on the R. They are surrounded by layers of fat and fascia and encased in a thick fibrous capsule
Blood supply kidneys
Supplied by renal arteries branching directly from the abdominal aorta distal to the SMA. They divide into segmental then to interlobar to arcuate and finally to interlobular arteries.
The afferent arteriole is crucial in regulating the volume of blood delivered to the nephron. It forms an extensive capillary network where the
- Vasa recta supplies the inner 1/3 of the cortex + medulla
- Outer 2/3rd of the cortex is supplied by the peritubular network
These the form the efferent artiole via via the renal veins drains directly into the IVC
Filtration @ Bowmans Capsule
Hydrostatic pressure forces fluid out. The filtration barrier consists of fenestrated endothelium with 60-80nm sizes pores on top of this sits the -vely charged GBM so large molecules such as albumin are retained. Podocytes foot processes form an interdigitated 40nm filtration slit
Juxtaglomerular apparatus
Regulates flow and filtration to each nephron. Column cells in the macula densa sense the concentration of Na+ in the tubular fluid. They can trigger adenosine mediated vasoconstriction of the afferent arteriole to reduce eGFR and retain more sodium and hence increase BP. This is mediated by renin and aldosterone
Endocrine function of the Kidney
Epo, renin via juxtaglomerular apparatus, 1a hydroxylation of vit D
Proximal tubule
Glucose and 80% of Na reabsorbed via Na+/Glucose co transporter. Cl- is reabsorbed to maintain electric neutrality. Na+/H+ exchanger allows HCO3 formed from c02 and h20 by carbonic anhydrase to be reabsorbed
Thick descending loop of Henle
H20 reabsorbed giving hypertonic urine
Thick ascending loop
Na+/K+/2Cl- symporter
Distal convoluted tubule
Ca2+ reabsorption mediated by PTH, Thiazide dependent Na+/Cl- transporter
Collecting duct
ENaC aldosterone mediated Na+ exchanged for K+ and H+
ADHs stimulates aquaporin insertion and h20 retention
Autocrine functions
Autocrine = actions on self
Endothelins = vasoconstrictors Prostaglandins= act to maintain renal blood flow in the face of angiotensin II and adrenergic stimulation ANP = Secreted from the cardiac atria in response to stretch produce Na+ excretion, lower BP and reduce renin and aldosterone secretion
Renal Hx
PMHx = gout, HTN, DM
Childhood UTI = vesicouteric reflux
Hx of renal stones or cystitis
Dix = Abx, NSAIDs, methotrexate, gentamicin/vancomycin
Nephritic syndrome
Inflammation leads to reactive cell proliferation and breaks in the GBM. Crescent forming. PC = haematuria and red cell casts
Causes = anti GBM (goodpastures), Vasculitis, post strep glomerular nephritis. SLE and IgA can
Nephrotic syndrome
Injury to podocytes leading to changed architecture and scarring. PC = oedema, hypoalbuminea, proteinuria and hypercholesterolemia
Causes = minimal change disease, FSGS, diabetic nephropathy, amyloidosis
Iga and SLE can
O/E renal disease
Parlour, fatigue and SOB ?anemia due to low epo
Purpuric rash, epistaxis, wt loss, arthralgia ?vasculitis
Palpable bladder ?retention/cancer
Palpable kidney ?ADPKD, transplat @ iliac fossa
Oedematous = nephrotic syndrome
Renal bruit ? renal artery stenosis
eGFR
Clinically used to assess degree of renal impairment (Not useful in acute setting). Uses for drug dosing and ESRF
Calculations take into account age, weight, race and serum creatinine
Limitations of eGFR
Too pessimistic in mild renal failure, most elderly patients are in stage III CKD yet have no impairment on their lives
Creatinine clearance
Produced by skeletal muscle filtered freely at the glomerulus with only a small amount secreted in the proximal tubule. Creatinine levels vary with muscle mass, activity and gender
Equation for creatinine clearance
(140-age x wt x constant)
Serum creatinine
Constant = 1.04 females, 1.23 males
Myeloma screen
CRAB symptoms. Serum free light chains/electrophoresis
Glomeluronephritis screen
ANCA (PR3 and MPO), anti-GBM, complement, ANA, dsDNA
Urine dipstick
Colour - haemturia? nephritic syndrome or myoglobin
Glucose - very sensitive indicated DM
Proteinuria - common sometimes benign (postural, exercise and pyrexia)
If two +ve dipsticks for protein offer ACR
Causes of Haemturia
Intra-renal = TIN, papillary necrosis, GN, Cysts, RCC, trauma
Extra-renal = ureteric stones, bladder cancer, infections, BPH, parasites, urethral trauma
False +ve = myoglobin, rifampicin, porphyria
Glomerular disease
Red cell casts, haematuria and proteinuria
Inv Renal
USS - safe, non invasive so imaging of choice allows visualisation of stones, assess size and symmetry of kidneys, characterisation of renal masses as cystic or complex and solid, guided biopsy, renal artery patency with duplex
Glomerulus structure
Network of capillaries at the beginning of the nephron
i) Fenestrated endothelium have large pores 50-100nm allowing passage of small molecules but not protein or RBC
ii) GBM strong collagen matrix with heparan sulphate giving -ve charge to repel albumin.
iii) Podocytes attach to the GBM by foot processes, adjacent podocytes are joined by slit diaphragms creating a sieve
Glomerulus in disease
Effacement of for processes leads to disruption is architecture of the filtration slit this may manifest as proteinuria.
Tubular disease
White cell casts, minimal proteinuria
Classification of glomerular disease
a) Nephrotic = massive proteinuria, oedema and hypoabluminemia due to podocyte injury
b) Glomerulonephritis = nephritic syndrome
Acute = abrupt onset haematuria, red cell casts and transient renal impairment
RPGN - acute nephritis, focal crescent necrosis and ESRF
c) Mixed nephrotic/nephritic = SLE, IgA, HSP
d) Asymptomatic proteinuria/haematuria
Causes of proteinuria
Glomerular in origin >1g
- Diabetic nephropathy, minimal change, FSGS, membraneous GN
- SLE and amyloidosis
Tubular in origin < 1g
ATN/ITN
UTI, ureteric stones
Bengin = fever, exercise and postural
Nephrotic syndrome
Massive proteinuria >3.5g a day may PC as frothy
Hypoalbuminemia <35g/l
Gross oedema = periorbital, ascites, ankles
Dyslipidemia
Complications of nephrotic syndrome
Can cause progressive renal failure
Hyperlipidemia - low levels of albumin lead to hepatic compensation by producing lipopoteins. Apolipoproteins are lost in the urine leading to reduced lipid catabolism and action of lipoprotein lipase. If prolonged = acceleration of CVD and atherosclerosis
Thrombophila - antithrombin III lost giving hypercoaguable state = increased DVT/PE risk
Infection risk due to loss of immunoglobulins
Causes of nephrotic syndrome
1 - minimal change disease, FGGS, membranous nephropathy
2 - SLE, amyloidosis, diabetic nephropathy
Minimal change disease PC
Seen commonly in children approx 20% causes of adult nephrotic syndrome. PC = facial oedema, selective protein loss albumin > immunoglobulins
Glomeruli appear normal on light microscopy however on electron microscopy fusion and effacement of the foot processes can be seen.
Causes of minimal change
Idiopathic - majority!
Hodgkin lymphoma, drugs - NSAID’s, ABx, HBV and HCV
Mx minimal change
Good prognosis <10% progress to ESRF. Steriods
Focal segmental glomerulosclerosis (FSGS) PC
Sclerotic glomerular lesions which affects some glomeruli and certain segments in each tuft. Evidence of hylanosis
Increased incidence in afro-carribeans
PC = massive proteinuria (no selective), HTN and haematuria
Inv and Mx for FSGS
Immunohistochemistry shows IgM and complement deposition
Biopsy = diagnostic
Mx = steroids and cyclophosphamide. 50% progress to ESRF @ 10yrs
Membranous glomerulonephritis
30% of adult nephrotic syndrome. Male predominance AI condition where autoantibodies target the GBM. Sub endothelial deposits activate the complement system which leads to damage to podocytes and mesangial cells
Haematuria referral
2wk wait if visable haematuria > 45y/o in absence of UTI
inviable haematuria >60y/o
IgA nephropathy
Most common form of glomerulonephritis worldwide caused by deposition of IgA complexes in the mesangium
IgA nephropathy
Most common form of glomerulonephritis worldwide caused by deposition of IgA complexes in the mesangium. This leads to proliferation and synthesis of mesangial matrix. Activation of complement and macrophage infiltration lead to glomerular injury
PC IgA nephropathy
Typically in childhood or young males post URTI or GI infection within a week. Microscopic or macroscopic haematuria.
Rapid recovery
Inv and Mx IgA
Biopsy shows mesangial proliferation and complex deposition. IgA on immunohistochemistry
USS to rule out obstructive cause
Mx = ACEi, steroids if needed
Thin basement membrane disease
AD condition typically presents with persistent microscopic haematuria + red cell casts.
Inv = Biopsy shows thinning of membrane due to collagen defect
Alport syndrome
X-linked disorder of type IV collagen which is found in the ears, glomerulus and eyes. This non functioning collagen undergoes progressive sclerosis = renal failure
PC = progressive proteinuria and haematuria, sensorineural hearing loss. 20% optic defect including anterior lexicons, myopia and corneal erosions
Diuretics
Loop - Furosemide acts block Na+/K+/Cl- transporter in the loop of Henle = potent effect
Thiazide - Bendroflumathiazide acts to block Na+/Cl- cotransporter in DC. Cause more urinary retention, glucose intolerance and hypokalemia than Loop.
Potassium sparing diuretics reduced Na+ reabsorption in exchange for K+ retention = spironolactone
Causes of membranous glomerulonephritis
1 - idiopathic 80%
2 - AI (SLE, thyroid, sarcoidosis)
Infections - HBV, HCV,
Cancer - lung, breast, colon + lymphoma
Drugs - gold, NSAIDs, penicillamine!!
Inv and Mx of membraneous glomerulonephritis
Invx - biopsy shows classic spike and dome pattern , IgG and C3 on immunofluorescent
Mx 1/3 = ESRF
Mx Nephrotic syndrome
LMWH tinzaparin to reduce risk of VTE
Statins for dyslipidemia
ACEi for proteinuria and HTN
Oedema = rest, fluid and Na+ restrict
Find and treat the cause!!
Myelomas = serum free light chains, Vasculitis ANCA +ve, anti-GBM, SLE =dsDNA
Biopsy is often needed for diagnosis
Glomerulonephritis
i) Non proliferative = nephrotic syndrome
Minimal change, FSGS, Membranous
ii) Proliferative GN = usually nephritic syndrome + crescents
IgA, post streptococcal, Membroproliferative
RPGN - anti-GBM and Vasculitis
Diabetic nephropathy
Glomerular hyper filtration leads to GBM thickening and mesangial proliferation - proteinuria occurs as filtration pressure rises and podcytes deplete.
In late stages of disease glomerulosclerosis occurs with with Kimmelstiel-Wilson lesion and hyaline deposits in the glomerular arterioles
ACEi
Mx diabetic nephropathy
Aim for good glycemic control, BP <120/80 with ACEi, control dyslipidemia
Nephritic syndrome
Haematuria + red cell casts on microscopy, HTN, proteinuria <3.5g daily, oliguria and progressive renal failure in some cases
Causes of nephritic syndrome
Post streptococcal, IgA, infective endocarditis
RPGN - HSP, Vasculitis, anti GBM, SLE
Post-streptococcal GN
Occurs in childhood often 1-3wks after a streptococcal infection often - otitis media, cellulitis or sore throat
Produces streptolysin leading to RBC haemolysis. Type III hypersensitivity deposition of complex in sub endothelium.
Inv - low complement, IgG and C3 deposition on biopsy
Membranoproliferative GN
Can present as mixed nephritic and nephrotic syndrome
Biopsy shows thickened capillary loops, diffuse thickened mesangium and IgG deposits. Tram track appearance
Linked to hep C
Mx = most pt develop ESRF
Stage I AKI
Creatinine rise > 26.4,
Creatinine 1.5-1.9x baseline
Urine output below 0.5ml/kg <12hrs
Stage II AKI
Creatinine 2.0-2.9x baseline
Urine output <0.5ml/kg > 12hrs
Stage III AKI
Creatinine rise >354
Creatinine 3x baseline
Urine output <0.3ml/kg for 24hrs or anuria
AKI
Very common 18% of A&E admissions linked to high mortality and long admissions. 50% of patients with sepsis will have an AKI
Crucial to distinguish AKI from CKD. Baseline creatinine, symptoms and duration.
Functions of the kidney
Endocrine = renin, epo and vit D hydroxylation
Excretion of waste urea, nitrogen and drugs
Fluid balance reabsorption of K+, P04, Ca2+
Pre Renal AKI
Hypoperfusion of the kidney leads to compromised renal function. This occurs when the usual mechanisms that autoregulate the GFR fail If this persists can lead to ischemia and ATN. This causes approx 80% of AKI
Causes of hypoperfusion
Hypovolemia = Burns, D/V, haemorrhage
Low cardiac output = MI, acute HF, PE
Vasoconstrictors = NSAIDs, ACEi
Distributive = Sepsis, hepatorenal, anaphylaxis
NSAIDs and ACEi
NSAIDs acts to inhibit prostaglandin production, they are essential to vasodilate the afferent arteriole. Hence NSAIDs lead to vasoconstriction of the afferent arteriole and reduced blood flow to the glomerulus
ACEi this act to block the effects of angiotensin II a potent vasoconstrictor of the efferent arteriole. They lead to reduced glomerular pressure hence low GFR
Intrinsic AKI
90% due to ATN
Acute tubular interstitial nephritis
Vasculitis, RPGN, ITP,HUS
Acute tubular necrosis
Necrosis of tubular cells due to
i) Prolonged ischemia
ii) Nephrotoxins - constrast, aminoglycosides, myoglobin
Pathology of ATN
Tubular injury leads to necrosis and apoptosis of the tubular cells, the tubules are then obstructed by the accumulation of necrotic cells leading to increased pressure in the tubules and reduced GFR
Tubular obstruction
Myeloma - paraproteins
Tumour lysis syndrome - urate
Rhabdomyolysis - myoglobin
Agglutination of proteins leads to tubular blockage and reduced GFR
Acute allergic interstitial nephritis
Rare. 80% of cases due to drugs. Rapid influx of inflammatory cells into interstitium
PC = may be asymptomatic, can present with a rash, fever, arthralgia and oliguria
Inv - biopsy shows eosinophils with variable tubular necrosis. Eosinophilia and eosinophiliuria
Mx stop the drug and steroids
Rhabdomyolysis
Causes - compartment syndrome, crush injuries, status epileptics, statins, long lie, excess exertion
Rapid rise in CK, K+, lactate and phosphate
Causes of TIN
Drugs - NSAIDs, Abx - penicillin, cephalosporins, quinones, carbamazepine, allopurinol, PPI, valproate, loop and thiazide diuretics
Can be due in infection or idopathic
RPGN
Mass proliferation of Bowmans capsule and rupture leading to crescent formation
- anti GBM (If lung involvement = Goodpastures)
- Immune complex deposition SLE, IgA, HSP, endocarditis
- Vasculitis
GPA
PC = sinusitis, nasal polyps, c-anca and PR3 +ve
EGPA
PC = asthma, eosinophils on biopsy, p-anca and MPO +ve, commonly anca -ve
MPA
PC = no granulomas on biopsy, p-anca and MPO
Anti GBM
20% of RPGN. If associated with pulmonary haemorrhage = Goodpasture’s. Anti-GBM antibodies present in serum and detected by ELISA and are directed against type 4 collagen in the BM
Cholesterol embolisation syndrome
Occlusion of micro vessel by cholesterol emboli from atherosclerotic lesions. Usually post op or angioplasty. Increased risk with anticoagulation
Haemolytic ureamic syndrome (HUS)
Characterised by intravascular haemolysis with red cell fragmentation, thrombocytopenia and AKI
Diarrhoea HUS (E.coli 0157)
PC = bloody diarrhoea and abdo pain due to E.coli strain that produces a shiga toxin that destroys RBC. Renal failure occurs due to blockage of tubules with schisctocytes
Mx = can be very severe 5% die, 20 may need dialysis, 30% residual renal impairment
Post renal AKI
Due to blockage of the ureter, bladder or outflow tract. If unilateral pt must have some pre-existing renal impairment. USS is crucial to identify cause
Causes of post renal AKI
Stones or neoplasms blocking ureter BPH Bladder cancer Urinary retention due to UTI/constipation Strictures
PC of AKI
Hyperkalemia - K+ is excreted by the kidney, can present as muscle weakness and palpitations leading to ECG abnormalities and arrhythmias
- ECG = tall tented T, flattened P, widened QRS
Mx = calcium gluconate, 100ml 20% dextrose and 10U insulin, Neb salbutamol
Metabolic acidosis due to reduced excretion of H+ ions
Fluid overload and pul oedema due to Na+ and hence h20 retention
Accumulation of urea = impaired haemostasis, N/V, drowsiness, fits, confusion, asterxsis, pericarditis
Pre-renal Hx and O/E
Hx - diarrhoea, bleeding and vomiting, symptoms of infection i.e. fever, cough, SOB, dysuria, fall and long lie
O/E - septic shock = warm peripherally, normal CRT,
cardiogenic = cold peripherally, hypotensive, JVP
Signs of infection crackles on auscultation
Intra-renal Hx and O/E
NSAIDs, Abx = TIN, Contrast recently? CRAB symptoms ?Myeloma Diarrhoea, purpura, young child ?HUS Wt loss, epistaxis, haemoptysis, fever etc ?Vasculitis Confused, fall = rhabdomyolysis
Post-renal Hx and O/E
Obstructive symptoms = gradual poor flow, dribbling, incomplete voiding, nocturia
Loin pain and frank haematuria, smoking ? TCC
Bladder palpable = urinary retention
PR ? BPH smooth enlarged vs prostate cancer hard nodular and craggy
Indications for acute dialysis
Hyperkalemia >7.0mm Ureamic encephalopathy Refractory pul oedema Severe metabolic acidosis Poisoning - aspirin
Inv AKI
Pre-Renal causes often on clinical signs and symptoms. Catherise to monitor urine output/ if in acute retention
USS to rule out post-renal causes
Urine dip for infection
ECG crucial to monitor for arrythmias
U+E, coat screen, ABG, CRP
Urine microscopy = red cell casts glomerular damage
Intrinsic screen
Serum free light chains = myeloma anti-GBM = Goodpastures dsDNA and low complement = SLE Blood film = HUS ANCA = vascilitis
Mx AKI
Treat oedema, hyperkalemia and uraemia as they present
Stop all nephrotoxic drugs - NSAIDs, ACEi, certain ABx
Adjust medications that will accumulate in renal failure - opioids and metformin
Fluid replacement stat. Let urine output guide
When to suspect 2ndary HTN
Young pt <40y/o
No sign of underlying cause i.e. - obesity, DM, FHx
Refractory HTN despite compliance
Primary hyperaldosteronism
Screening with a aldosterone:renin. If high indicates causes. Adrenal vein sampling may be required to decide whether Conns vs bilateral hyperplasia
Phaechromocytoma
PC = headache, sweating, tachycardia, HTN Inv = plasma metaephrine level
Linked to MEN2, von hippel landau and NF1
Acromegaly
PC = large feet and hands, carpal tunnel, macroglossia, spaced teeth, OSA, DM. 95% due to pituitary adenoma may - tunnel vision and headaches
Cushings syndrome
PC = striae, hirsutism, facial plethora, central obesity, osteoporosis, DM, proximal myopathy
Inx = urinary free cortisol or low dose dex
Plasma ACTH levels
High dose dexamethasone
Atherosclerotic renovascular disease (ARVD)
Atherosclerosis 16% of patients > 60. Pt with co-exisiting PVD, CCF are at increased risk.
PC = often asymptomatic. HTN in 50%, Na+ retention may precipitate flash pul oedema. Renal bruit. Small kidney on USS
Mx ACEi may precipitate AKI GFR will fall by 30% and then stabilise. If >75% stenosis
Renal artery stenosis
ARVD or fibromuscular dysplasia
The effected kidney has reduced perfusion leading to chronic RAS activation. Renin production and aldosterone release to retain Na+ and h20. Effected kidney produces more concentrated urine and has a lower GFR
Inv - USS and MR angiogram
Mx renal artery stenosis
wt loss, control cardiac factors. ACEi
Revascularisation
When to revascularise in renal artery stenosis
Stenosis >75%, declining renal function, single kidney, flash refractory pulmonary oedema, severe HTN,
Fibromuscular dysplasia
Rare - presents in young women with HTN and renal bruits. Can present at the carotid or coronary arteries
MRI = string of beads appearance
HTN in hyperparathryoidism
Increased intracellular Ca2+ SM contraction in arterioles increasing PR
Pathogens causing UTI
E.coli, proteus, stap saprophyticus, enterococcus
Risk factors for UTI
Female, stones, sexual activity, indwelling catheter, DM, urinary tract stasis, dementia
PC UTI
fever, dysuria, polyuria , smelly urine and haematuria.
Causes of HTN in CKD
Impaired Na+ excretion leads to sodium retention and expansion of the extracellular volume. Activation of RAS leads to direct vasoconstriction to aid Na+ retention.
CKD definition
Kidney dysfunction >3months. Albumin:creatinine >3mg/mmol, falling GFR <60, rising creatinine
Causes of progressive CKD
HTN, DM, Urinary obstruction i.e. stones, BPH, recurrent UTI, Glomerular diseases = SLE, amyloidosis, Vasculitis. Nephrotoxic drugs
Prognosis of CKD
Depends on eGFR and ACR
Poor prognosis if ACR >30
Stages of CKD
I >90 II 60-80 III a - 45-59, b - 30-44 IV 15-29 V <15
PC CKD
Progressive asymptomatic decline in eGFR. Comorbidity such as DM, HTN, AI conditions. As renal function declines will lead to anaemia, electrolyte disturbances, fluid retention, HTN, restless legs and neuropathy,
Progression of CKD
In CKD many of the nephrons are scarred and have failed, hence their job of filtration falls on the remaininf nephrons. This hyperfiltrative state imposed on the remaining nephrons despite no increase in renal blood flow leads to hypertrophy and reduced arteriole resistance. The increased flow and pressure perpetuates the system.
Inv CKD
U+E, ACR, urinalysis.
USS to rule out reversible causes, if acute ?renal artery stenosis
Urine dip and microscopy - red cell casts ?GN, eosinophilia?TIN
Fragmented red cells +/- low platelets ?HUS/TTP
ANCA ? vasculitis
Mx CKD
BP control <140/90 unless DM <130/80 ACEi Low salt diet, fluid restriction Reduce wt, stop smoking, CVD risk?statin Monitor K+/urea levels Hyperphosphatemia due to inability to secrete and cant hydroxylated vit D = hypocalcemia and possible 2ndary hyperparathryoidism Epo if anaemia
Uraemia complications
Ureamic pericarditis
Uraemic encephalopathy
Bleeding
Bone disease in CKD
Spectrum can encompass osteomalacia, hyperparathyroid and osteoporosis
Phosphate excretion falls. Secondary hyperparathyroidism develops as renal function declines production of 1ahydroxylase leads to less active vit D so reduced GI calcium absorption. Trigger PTH release to increase Ca2+ blood levels caused by phosphate retention and reduced GI absorption.
2ndary hyperparathyroidism in response to low Ca2+leads to increased osteoclastic actitvity, cyst formation and osteitis fibrosis cystica. Inv = high PTH, low Ca2+, high PO4 and high ALP
Tertiary hyperparathyroidism
Chronic hypocalcaemia leads to autonomous production of PTH by the parathyroid gland. Acts independently = high Ca2+, high PTH
Mx bone disease in CKD
Phosphate binders and novel vit D metabolites
Haemodialysis
Relies on a machine to monitor pressure, LMWH for anticoagulation, air trap to prevent air embolisms. Blood is passed in a countercurrent system through a semi-permeable membrane against dialysis fluid which is low in Na+, K+, urea, H+ allowing toxic metabolites to diffuse down concentration gradient
Pros and cons of haemodialysis
-ve = restriction on life 3x weekly 4hrly sessions, pt tired after, can = hypotension due to large volume of fluid removed
AV fistula
Created by anastomosing the brachial artery and cephalic vein. Takes 6 weeks to prepare. Veins walls thicken under arterial flow allowing repeated use, arterial blood flow needed for dialysis
O/E - thrill and bruit due to turbulent flow, often engorgement of veins in arms
AV fistula pros and cons
+ve = higher flow rates gives more effective dialysis, lower risk of infection and thrombus
-ve = steal syndrome leading to cold extremities and cramping pains. Aneurysm formation
Central venous catheter
Plastic catheter with 2x lumen inserted into large vein usually IVC or femoral. Tunnelled under the skin
They have an increased risk of infections compared to fistulas can lead to stenosis and occlusion of the veins with repeated use due to scaring and fibrosis.
Aim of dialysis
Maintain euvolemic, prevent acidosis and hyperkalemia
Peritoneal dialysis
Uses the peritoneum as a semi-permeable membrane, permeant catheter is inserted allowing fluid to be administered daily
Pros and cons of peritoneal dialysis
\+ve = increased independence, can be done overnight -ve = bacterial peritonitis = fever, cloudy dialysate fluid, abdo pain. Hernias, catheter site infections.
Serious = sclerosing peritonitis leading to adhesions and strictures causing repeated small bowel obstruction
Transplant
Treatment of choice. New kidney lasts 10-15yrs. Improved QoL, cost effectiveness, mortality benefit, correction of metabolic problems
CI to renal transplant
Cancer, severe heart disease, active infection, low performance status
Types of renal transplant
Living donor via paired pool exchange
Deceased donor
i) DBD = better prognosis due to increased perfusion
ii) DCD
Mx renal transplant
HLA matching crucial!!
Steroids, antimetabolites = MMF/azothioprine,
calcinerin inhibitors = tacrolimus
Red cell casts and white cell casts
Red cell casts = glomerular pathology - vasculitis, anti-GBM, SLE, post strep GN, endocarditis, renal infarction
White cell casts = TIN, nephrotic syndrome and pyelonephritis
Cresentric glomerulonephritis
Indicates severe acute renal damage. Starts with a gap in the glomerular capillary wall and GBM. Inflammatory mediators move into Bowmans space. T-cells and fibroblasts proliferate
%age of glomeruli with crescents linked to recovery and prognosis
Tacrolimus/ciclosporin
Calcineurin inhibitors disrupt T cell signalling
Azathioprine/MMF
Inhibit purine synthesis hence the active proliferation of lymphocytes
