chronic kidney disease Flashcards
what is the definition of CKD?
the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated GFR that persists for more than three months.
OR in short
Abnormal kidney structure or function, present for >3 months, with implications for health.
what are the causes of CKD?
- Diabetes
- Hypertension
- Glomerulonephritis
- Renovascular Disease
- Polycystic Kidney disease
- Obstructive nephropathy – urological problems
- Chronic/recurrent Pyelonephritis
- Others
what are the complications of CKD?
- Anaemia of Chronic Kidney Disease
- Chronic Kidney Disease – Mineral & Bone Disease
- Secondary & Tertiary Hyperparathyroidism
- Hypertension
- Cardiovascular Disease
- Malnutrition/sarcopenia
- Dyslipidaemia
And, as CKD progresses
- Electrolyte disturbances
- Fluid overload
- Metabolic acidosis
- Uraemic pericarditis
- Uraemic encephalopathy
how is CKD stage categorised?
can be done based on
- GFR
- the presence of albuminuria as a marker of kidney damage
- the cause of kidney disease
how does GFR correlate to stage of CKD?
Stage 1 = GFR>90 (only CKD if other evidence of kidney damage)
Stage 2 = GFR 60-89 (same as above)
stage 3a = GFR 45-59 (mild-moderate)
stage 3b = GFR 30-44 (moderate=severe)
stage 4 = 15-29 (severe)
stage 5 = <15 (kidney failure)
what would the MDT consist of in CKD management?
- Renal Physicians
- General Practitioners
- Renal Specialist nurses/ Home Care team
- Dieticians
- Pharmacists
- Vascular/Transplant Surgeons
how is a CKD patient managed as an outpatient?
- treat underlying disease e.g diabetes, hypertension
- treat infections promptly
- if they have autosomal dominant polycystic kidney disease, tolvaptan can be given
- immunosuppression for GN if appropriate
- reduce CV risk e.g statin, control bp and DM, and lifestyle changes
- reduce CKD progression e.g reduce proteinuria with ACEi/ARB, monitor bloods and control BP
- prevent/ treat complications of CKD e.g dietary advice for low phosphate/K diet. IV iron/folate/vit b12, EPO, vit D supplements, phosphate binders and dietician input.
how can you plan for the future with a patient with CKD?
- Start discussions of what options they have if they
reach ESRF - Home care team input
- Discuss disadvantages & advantages of types of
RRT e.g
1) home therapies – APD, CAPD, Home HD
2) Unit-based therapies – Nocturnal HD, conventional HD
3) Active conservative management
3) Transplant
- Refer for fistula (venous mapping)
- Refer for PD tube insertion
- Work-up for transplant (Further tests and refer to Transplant work-up clinic)
how can diabetic neuropathy result in CKD?
Type 1 DM or long standing Type 2. Most diabetic patients will undergo screening for diabetic nephropathy and will have
- Raised Urine Albumin: Creatinine Ratio/PCR
- Evidence of long-standing/poorly controlled DM
- Evidence of other microvascular disease e.g retinopathy or peripheral neuropathy
how is diabetic nephropathy treated?
- ACEi/ARB to reduce proteinuria
- Anti-hypertensives for BP control
- Cardiovascular risk modification
- Continue other screens for microvascular complications – eye checks and foot checks
how does hypertensive nephropathy come about?
Chronic raised BP causing nephrosclerosis.
Often difficult to tell if advanced renal disease at presentation whether HTN caused the renal impairment or renal impairment caused secondary HTN
what investigations can be done to identify primary or secondary HTN and how is it treated?
- 24 hour Urinary metanephrines (Phaeochromocytoma)
- Aldosterone: Renin ratio (high in Primary aldosteronism aka Conn’s syndrome)
- Cortisol & Dexamethasone suppression test
(Cushing’s syndrome) - TSH (hyperthyroidism)
- MRA (Renal artery stenosis)
treat with antihypertensives
how is polycystic kidney disease diagnosed and treated?
Diagnosis
- FH
- USS
Treatment
- Control BP
- As per CKD management
- Tolvaptan (Vasopression receptor-2 antagonist) is
available for some patients to slow progression of
CKD. - Genetic counselling and testing
what are the symptoms of Polycystic kidney disease?
Symptoms can be related to the size of the kidney, infection of the cysts (flank pain, haematuria, and fever) or can be asymptomatic
what genetic mutations are present in polycystic kidney disease?
Type 1 (85%; PKD1 mutation on Chromosome 16)
Type 2 (15%; PKD2 mutation on Chromosome 4)
how do you get anaemia of CKD?
- Decreased production of erythropoietin from the kidney
- Absolute iron deficiency (poor absorption and malnutrition)
- Functional iron deficiency (inflammation, infection)
- Blood loss
- Shortened Red Blood Cell survival
- Bone marrow suppression from uraemia
- Medication induced
- Deficiency of Vit B12 and folate
how is anaemia of CKD managed?
1) Measure haematinics – Vitamin B12, Folate, Ferritin, Iron, Transferrin Saturation, CHr
2) If deficient in any of above – replace this first
(IV Iron may be better tolerated than PO)
3) Discuss with renal team regarding starting ESA Aim for Hb 100 - 120
how can CKD mineral bone disease be diagnosed?
if a patient with CKD has evidence of one or more of:
1) Abnormalities of calcium, phosphate, alkaline phosphatase, PTH or vitamin D metabolism
2) Vascular and/or soft tissue calcification
3) Abnormalities in bone turnover, metabolism, volume, linear growth or strength
what are some low and high bone turnover states?
Low turnover states
- Adynamic bone disease
- Osteomalacia
High turnover states
- Osteitis Fibrosa
how can CKD affect levels of
- fibroblast growth factor 23
- alkaline phosphatase
- PTH
- phosphate
- serum calcium
- 1,25 vit d
- Increased Fibroblast Growth Factor-23
- Increased Alkaline Phosphatase and PTH
- Increase Phosphate
- Decreased Serum Calcium
- Decreased 1,25 – Vitamin D as there is reduced hydroxylation of vit D
what is territory hyperparathyroidism?
Occurs when PTH release continues despite raised serum Calcium levels (independently)
- As a result of parathyroid gland nodular hyperplasia
- Consequence of advanced CKD
results in mineral bone disease
what is the relation between PTH and calcium?
PTH released from parathyroid causes Ca release from bones. Ca increase in blood goes to parathyroid and reduces PTH release.
PTH also aids calcium reabsorption for the kidneys and the intestines
how is CKD mineral bone disease managed?
Focus is to reduce:
(1) The occurrence and/or severity of renal bone disease
(2) Cardiovascular morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload.
On examination, what will be observed in CKD?
- peripheral oedema
- signs of peripheral vascular disease/ neuropathy
- yellow tinge (uraemia)
- xanthelasma
- signs of anaemia
- periorbital oedema in nephrotic syndrome
- stigma of endocarditis
- pulmonary effusion or oedema
- PD catheter or scars from previous catheter
