Renal

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Chronic Kidney Disease +/- Dialysis


Presentation and diagnosis
  • Symptoms of CKD are non specific
  • edema, hypertension, and/or decreased urine output
  • More significant: weakness and easy fatigability, anorexia, vomiting, mental status changes, and seizures
  • Disease specific - eg ANCA associated vasculitides, lupus, IgA nephropathy following an upper respiratory tract infection, TTP etc
  • Ix include serology, imaging +/- biopsy, proteinuria, casts etc
Risk factors
  • T2DM, hypertension, analgesic consumption, gout, vasculitides, idiopathic glomerulonephritis, amyloid, sarcoid, renal vascular disease
Complications
  • anuria and symtoms of fluid overload
  • uraemic complications - itch, encephalopathy, neuropathy, pericarditis, lethargy
  • hypertension 
  • anaemia, usually multifactorial - Fe deficiency if having uraemic bleeding, haemolysis, EPO deficiency, BM supression, aluminium toxicity
  • Bone disease - renal osteodystrophy, adynamic bone disease, osteoporosis, osteomalacia
  • Metabolic complications - hyperkalaemia
  • Cardiovascular complications
Management:
  • Goals of therapy are to (1) confirm diagnosis (2) optimise symptoms (3) reduce progression (4) manage complications (5) Treat specific cause (6) Ensure appropriate follow-up
  • Confirm diagnosis with the necessary investigations
    • all patients should have kidney US, basic blood tests, urine casts, microscopy, active sediment, albumin creatinine ratio
  • Optimise symptoms
    • General non-pharmacological strategies
      • Kidney Health Australia has a suite of brochures, health fact sheets, publications and self-management resources that give precise, up to date health promotion and disease prevention messages
      • Lifestyle interventions for targeted cardiovascular risk - remembering that CKD is a coronary artery disease risk equivalent more significant than diabetes itself
      • recommended that after GFR <30 one should see an accredited dietician
    • ​Neuropathic pain - massages, hot-cold compresses, anti-neuropathic agents such as pregabalin
    • muscle cramps - massages, stretching exercises, tonic water may help
    • restless legs - massages, relaxation techniques, make sure Fe is replete, consider dopamine agonists 
    • anaemia - mentioned later
    • uraemia - dialysis, or if palliative approach then symptomatic management
  • ​Reduce progression
    • ​Treat specific cause eg lupus, ANCA vasculitis
    • Manage hypertension - target <140/90 in CKD, 130/80 in diabetes. Non pharmacological lifestyle methods such as increased physical activity within the limits of the patient, aim to initiate ACE-inhibitor/ ARB first - review after 2 weeks, if not below target then check compliance and optimise adherence, add calcium channel blocker or beta-blocker or diuretic, review after 2 weeks
    • Manage other cardiometabolic risk factors - consider statin if absolute cardiovascular risk >10% in 10 years, reduce smoking, aim for weight loss​ if overweight (4.4 mmHg for 5.1kg weight lost), adopt DASH diet (DASH diet: 5.5 mmHg for normotensives; 11.4 mmHg for hypertensives), Salt no more than 6g/d, increase physical activity to 30 mins mod intensity on almost every day of the week
  • Manage complications
    • Anaemia - target Hb 100 - 115, ferritin 200 - 500, transferrin sats 20 - 30%, EPO agents such as weekly aranesp, aim monthly increase of 10g/L, no quicker as get hypertension or seizures. EPOA can only be supplied by a nephrologist
      • Patient may have EPO resistant anaemia, therefore consider other causes
    • Acidosis - sodibic 840mg once daily to two tablets BD, titrate HCO3 > 22, care should be taken as it is a significant volume load
    • Bone health - low turnover osteomalacia, osteitis fibrosa, adynamic bone disease. Driven by raised PO4 and low activated vitamin D. Targets are PO4 [0.8 - 1.6], Ca 2.1 - 2.4, [Ca x PO4 < 4]
      • Control PO4 with dietary phosphate restriction and phosphate binders - calcium carbonate, sevelamer [for pt on dialysis], lanthanum [for pt on dialysis]
      • Use calcitriol (D3) or paracalcitol to titrate up calcium
        • Measure PTH 2-3 monthly
        • PTHectomy for autonomous i.e. high PTH and calcium, whilst off all calcium and vitamin D agents
      • Calcimimetics
        • Parthyroid sensitised to respond to lower calcium levels
        • No survival benefit but can decrease PTH, calcium and phosphate, [Ca x PO4}
    • Immunise against influenza and pneumococcus
    • Albuminuria - aim 50% decrease in ACr using ACE-inhibitors/ ARBS
    • Screen for depression
      • SSRIs (selective serotonin reuptake inhibitors) have established safety in people with CKD
    • ​Volume overload
      • ​may need more sessions of dialysis
      • Need very large doses of loop diuretics​​
    • ​Potassium
      • ​Target K < 6
      • Manage with low K diet, correct acidocis, avoid salt substitutes, cease potassium sparing diuretics
    • ​Nutrition
      • ​Target albumin > 35
      • when GFR < 30 --> refer to dietician
      • target 0.75-1g/kg protein
Dialysis specific management
  • Consider when GFR <20, and offered if pt expected to live > 1 year
  • Native AV fistula should always be attempted to be created, fistula's should be created distally in the upper limb if possible from the wrist (radiocephalic) working proximally (eg brachiocephalic). If a native graft cannot be fashioned, then a synthetic graft is preferred over a catheter. 
  • Patients using catheters, had higher risks for: all-cause mortality, risk ratio (RR) =1.53 (95%CI: 1.41-1.67, P<0.01); fatal infections RR = 2.12 (95%CI: 1.79-2.52, P = 0.82); and cardiovascular events RR = 1.38 (95%CI: 1.2-1.54, P=0.47) compared with individuals using fistulae. 
  • All patients, especially those with co-morbid conditions, should be referred to a vascular access surgeon well in advance of the anticipated need for haemodialysis. 
  • Primary determinants of mode of initial dialysis include the preference of a fully-informed patient, absence of medical and surgical contraindications, and resource availability​
  • When dialysis modality is not determined by preference of a fully-informed patient, absence of medical and surgical contraindications and resource availability, consider using continuous ambulatory peritoneal dialysis (CAPD) (not automated peritoneal dialysis [APD]) in preference to haemodialysis to better preserve residual renal function (RRF) and allow graded introduction of dialysis.​
  • Commence dialysis when GFR falls below approximately 10 mL/min/1.73 m2 if there is evidence of uraemia or its complications such as malnutrition. 
  • If there is no evidence of uraemia or its complications including malnutrition, commence dialysis when GFR falls below approximately 6 mL/min/1.73 m2 

Renal +/- Pancreas Transplant


History
  • Cause of CRF: eg T2DM, glomerulonephritis, reflux nephropathy, APKD
  • Pre-transplant evaluation
    • Tissue typing
      • ABO compatibility. Incompatibility obviously affects graft survival
      • Tissue typing (HLA A, B, DR)
    • cardiorespiratory status: intermediate risk --> stress test (dobutamine ECHO, stress MIBI), high risk --> coronary angiogram, ABG, pulmonary function tests
    • Nutritional status
    • Infection/ malignancy status, screening for absolute contraindications
      • active/ disseminated malignancy
      • uncontrolled/ untreated infection
      • chronic infection
      • unacceptable anaesthetic risk
    • Psychosocial:
      • adherence/ compliance
      • insight
      • MH comorbidities
  • Transplant Hx: Date, ABO match, HLA match, Living donor or decreased donor, CMV status of donor and recipient
  • Combined Kidney/ pancreas transplant
    • goals of transplantation --> restore glucose-regulated endogenous insulin secretion, arrest progression of diabetic complications, improve quality of life
    • Usually done in conjuction with renal transplant - in this setting it can mean that the transplanted kidney will survive longer
    • Could have pancreas only transplant if there is frequent, acute, severe metabolic complications (hypoglycemia, marked hyperglycemia, ketoacidosis), significant difficulty with insulin therapy, and consistent failure of insulin-based management to prevent acute complications
    • islet cell Tx still evolving, only done in clinical trials setting
    • high rate of insulin independence with pancreas Tx (graft survival 81, 55, and 51 percent at one, three, and five years)
    • Unique immunosupressive requirements with pancreas Tx --> tacrolimus instead of cyclosporin, mycophenolate instead of azathioprine
    • Episodes of rejection follow renal rejection
  • Surgical Hx: Intra-operative complications, ICU length of stay, tolerability of induction regime
    • Induction regime: Triple therapy + basiliximab (IL2 R antibody)
    • Maintenance: Triple or dual therapy
  • Complications: 
    • Rejection episodes
      • hyper-acute rejection may have complicated a previous renal Tx. This is rare and untreatable. This is due to preformed antibodies, and is predictable by cross matching process
        • This will lead to loss of graft
      • Acute rejection: diagnosed on biopsy, heralded by increasing serum creatinine, decreased urine output. Classically T cell mediated, broad DDx include ATN, drugs, obstruction, pre-renal impairment. Pathology is broken down into cellular (tubulitis, interstitial infiltrate), vascular (endothelialitis, glomedulitis, haemorrhage), antibody (PMNs, C4d+ staining). 
        • Cellular rejection: Rx 250mg-1g methylprednisone x 3-5 days, usually reverses 90% of acute rejection episodes, if steroid resistant may need anti-T cell antibodies (ATG, OKT3), these reverse 75% of steroid resistant rejection episodes, if still refractory, then can give high dose tacrolimus and mycophenolate
        • Antibody rejection: IVIG, Plasmapheresis
      • Chronic rejection: common, occuring in 30% of transplant Pts, of immune and non-immune aetiology, presenting with progressive renal dysfunction, proteinuria and hypertension
    • Infections in immunocompromised host
      • Prophylaxis: 
        • Valganciclovir prophylaxis for CMV+ recipient or CMV + Donor --> CMV - recipient Careful about chance of CMV disease
        • Bactrim prophylaxis for 6/12, if cannot tolerate this then nebulised pentamidine
        • Fungal prophylaxis with fluconazole
        • BK nephropathy: Occurs because BK virus reactivation occurs secondary to immunosupression, Found by decoy cells on urine cytology and BK virus PCR (urine/ blood), Rx by decreasing immunosupression
    • Declining renal function:
      • Broad differential, work through the causes and pre-test probability modified by timing post transplant. Differentiate into pre-renal, renal and post-renal causes
      • Immediate (<48h) - need to consider surgical causes strongly, but rejection and CNI toxicity also occur
      • Early (<4 weeks) - consider in addition to surgical causes haemolytic uraemic syndrome - look for evidence of a microangiopathic blood film (assoc with infection, CNI, mTOR toxicity, OKT3 use, acute vascular rejection, Rx with PLEX/ FFP). 
      • Late (>4 weeks): Consider all the above but also renal artery stenosis
    • Re-occurence of disease
      • Especially metabolic if not controlled and a number of glomerulonephritis
    • Drug side-effects:
      • Cyclosporin: MOA [binds to cyclophilins --> inhibits calcineurin which is a phosphatase --> number of transcription factors cannot translocate to nucleus --> reducing transcriptional activation of early cytokine genes for IL-2], therapeutic drug monitoring [troph, AUC, 2hr post dose], Toxicity [nephrotoxicity secondary to acute intra-renal vasospasm, chronic stripped fibrosis, TTP/ HUS, low Mg, neurotoxicity with tremor, Hirsutism, gingival hyperplasia ]
      • Tacrolimus: MOA [binds to FK506 --> inhibits calcineurin which is a phosphatase --> number of transcription factors cannot translocate to nucleus --> reducing transcriptional activation of early cytokine genes for IL-2], Toxicity [less nephrotoxicity, more post Tx DM, no gingival hyperplasia, less hyperlipidaemia, less HTN compared with cyclosporin]
      • Mycophenolate: MOA [Reversible inhibitor of inositol monophosphate dehydroganase (IMPDH) in purine biosynthesis --> lymphocytes can only synthesise purines through de-novo pathway and there is no salvage pathway + salvage pathway unaffected in other cells], largely replacing azathioprine with lower rates of rejection, toxicity [myelosuppression (more lymphopenia and anaemia, less thrombocytopenia), GIT (nausea and diarrhoea)]
      • mTOR inhibitors: These include sirolimus and everolimus. MOA [Bind FK binding proteins --> inhibit mTOR which is a kinase participating in downstream signalling through IL2R which is the third signal], not nephrotoxic, impaired wound healing therefore done use immediately post transplant, sirolimus pneumonitis, sirolimus has very long half life, metabolic side effects including dyslipidaemia
    • Bone health
      • Bi-annual BMD, may need bisphosphonates, keep Ca/ Vit D replete
    • Vascular risk factors and management
    • Malignancy surveillance
      • Dermatological, ensure age appropriate cancer screening is adhered to
Examination
  • SCC/BCCs
  • Cushing’s syndrome
  • Allograft site
  • Old/current AVFs
  • Examine mouth for candida and gum hypertrophy
  • Gouty tophi
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  • About
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    • Respiratory Medicine
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      • Colorectal Cancer
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    • Haematology >
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