Chronic Kidney Disease (Ckd)

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Introduction:

Chronic Kidney Disease (CKD is defined as a structural and functional abnormality of the kidneys persisting for 3 months or more and manifesting as markers of kidney damage or reduction in glomerular filtration rate (GFR).

Markers of kidney damage include persistent microalbuminuria or overt albuminuria or haematuria.

Structural abnormalities include
abnormalities on imaging or on histology.
CKD is also defined as GFR less than 60ml/min or presence of markers of kidney disease for 3 months or more.

Markers of kidney disease

These include:

  • Persistent proteinuria – Dipstick positive proteinuria or microalbuminuria
  • Persistent Haematuria – by dipstick and/or urine microscopy
  • Abnormal renal imaging by various techniques such as ultrasonography, Computerised Tomography Scan, intravenous urography or plain radiograph, renal scintigraphy.
  • Abnormal renal histology

Stages of Chronic Kidney Disease

The table below defines the 5 stages of CKD

[table “7” not found /]

Clinical Features

Asymptomatic

  • Younger patients may present with peri orbital swelling early in the disease process. Swelling which may then progressively worsen over time and lead to ascites and anasarca.
  • Hypetension develops in majority of patients with CKD
  • Congestive cardiac failure or cerebrovascular disease.
  • Reduction in urine output (oliguria)

Features of uraemia:

Gastrointestinal system

  • nausea, vomiting, hiccups, diarrhoea, epigastric pain and rarely haematemesis.
  • Chest central chest pain of pericarditis or breathlessness with development of pulmonary oedema.

Central nervous system

  • tremors
  • derangement of sleep rhytmn,
  • drowsiness,
  • seizures and stupor or coma.

Skin

  • dryness and pruritus

Haemopoietic system

  • anaemia (pallor) and
  • bleeding diathesis.

Diagnostic criteria:

  • As in the definition and table above.

Differential Diagnoses

  • Severe acute kidney injury with cortical necrosis
  • Poisoning with multiple organ involvement.
  • Chronic Congestive cardiac failure (Cardio renal syndrome).

Complications:

  • Anaemia
  • CKD Mineral and Bone Disease
  • Congestive cardiac failure
  • Cerebrovascular disease
  • Malnutrition
  • Peripheral vascular disease

Relevant investigations and management.

Urine Examination (Volume / microscopy
/Urinalysis / Electrolytes) Serum chemistry (e.g. creatinine, urea, K): This would

  • Allow estimation of GFR using various formulae and staging of the CKD
  • For planning or initiation of renal
    replacement therapy
  • To monitor treatment outcomes or improvement.

Haematology including serology:

  • To assess the Full Blood Counts, clotting profile and monitor response to treatment with ral or parenteral iron and Erythropoietin stimulating agents
  • Serological tests for HBV, HCV and HIV are necessary to be able to isolate infectious patients while applying general precautions in the management of all patients.

Imaging (e.g. USS, IVU, RUCG etc.):

  • Renal ultrasonography remains the simplest non-invasive diagnostic tool for patients with CKD.
  • This provides information on size, shape, preservation of cortical thickness and cortico medullary differentiation as well as echogenicity of the kidneys, which are usually deranged in patients with advanced CKD.
  • Other structural abnormalities like polycystic kidney disease or hydronephrosis may be  discovered and may suggest need for other imaging modalities particularly in patients with obstructive uropathy.

Renal biopsy:

  • Renal biopsy is mandatory in
    patients that present with some conditions. These include

Any evidence of glomerular disease

  • nephrotic range proteinuria
  • sub-nephrotic range proteinuria with or without haematuria
  • RBC cast
  • Presence of persistent microscopic haematuria
    • Suspicion of connective tissue. disease
    • Presence of familial type of nephrotic syndrome
    • Determine the prognosis and response to therapy.

Principles of management of patients with CKD include:

  • Counselling to discourage use of nephrotoxins in whatever form and ensure good compliance.
  • Good Blood Pressure control..
  • Reduction of proteinuria and ensuring maximum renoprotection
  • Maintenance of fluid homeostasis
  • Control of biochemical abnormalities
  • Maintenance of nutrition
  • Maintenance of haemoglobin between 11-12g/L
  • Maintenance of normal calcium phosphate homeostasis
  • Treatment of any complicating infection
  • Treat the underlying cause (more useful if discovered early)
  • Dialysis where indicated

What to do when CKD is detected:

  • Stage the disease
  • Take appropriate measures depending on the stage:

Stage 1 – 2 where the cause of CKD is
known, treat underlying cause and
institute measures to retard progression.
Stage 1-2: where cause is unknown, refer to Nephrologist.
Stage 3-5: refer to Nephrologist.

Treatment of hypertension:

Combination of different groups of
antihypertensive drugs is the rule but should include maximal doses of either ACEI or ARBs to achieve target BP.

Blood Pressure Targets:

Proteinuria <1g/24hrs =130/80mmHg
Proteinuria >1g/24hrs = 120/75mmHg
CKD with diabetes = 120/75mmHg
In children, less than 90 percentile for the age, sex and height.

Anaemia is the commonest haematological complication of CKD and worsens with deterioration of renal function.

All CKD patients should be screened for anaemia at time of diagnosis and thereafter, at least every 3 months.

Targets for anaemia treatment:

Predialysis: Hb: 11-12g/dl, serum ferritin: 100-500ng/ml, TSAT ≥20%

Dialysis: Hb-11-12g/dl, serum ferritin 200-500ng/ml, TSAT ≥20%

In all patients, avoid Hb level > 13g/dl
because of risk of haemoconcentration and its effect on morbidity and increased
cardiovascular mortality”.

Treatment of anaemia:

  1. In predialysis patients and patients
    receiving peritoneal dialysis or home haemodialysis, optimize iron balance before Epoetin therapy using oral iron.
    If poor response (TSAT is <20% and serum ferritin < 100ng/ml for 4 weeks), switch to parenteral iron.
    Dose of oral iron: Ferrous sulphate 200mg or Ferrous gluconate 600mg three times daily (approx. 65mg elemental iron) or 2 6 mg /kg /day of elemental iron for  paediatric patients.
    Dose of parenteral iron: Iron sucrose intravenously 200mg weekly for 5 weeks (total of 1000mg) or Iron dextran intravenously 250mg weekly for 4 weeks.
    For patients in whom adherence may be difficult, total dose infusion should be considered as its been found to be effective and safe.
  2. For patients on in-center haemodialysis, start with parenteral iron at 100mg in the last 30-60 minutes of the dialysis session to a total of 1000mg.
    In cases of poor or inadequate dialysis, higher doses may be given to ensure achieving 1000mg within 4 weeks.
    Test dose of iron dextran should be administered before the full dose. For patients that have received blood transfusions, check iron stores (serum ferritin) before giving supplemental iron because of risk of iron overload.
  3. Erythropoiesis Stimulating Agents (ESAS). These should be administered preferably after iron deficiency has been corrected and BP controlled.

Table 2: Types of ESAS and their characteristics.

[table “8” not found /]

Short acting ESAS – Epoetin alfa and
Epoetin beta.

Intermediate acting ESAs – Darbepoetin alfa

Long acting ESAS-CERA

Dialysis:

Based on manifestation of clinical and
biochemical features of uraemia or
development of electrolyte and acid-base
complications of CKD.

The clinical features include:

  • Encephalopathy,
  • Pulmonary oedema,
  • Persistent nausea and vomiting,
  • Pericarditis, refractory oedema,
  • Uncontrolled HT
  • Bleeding diathesis.

The biochemical indications include:

  • hyperkalemia >6.5mmol/l,
  • serum bicarbonate <12mmol/1,
  • urea > 25 mmol/l,
  • creatinine >600micromol/1

Manifestations of features of hypercatabolism:

  • K+ rate of rise >1mmol/day
  • urea rate of rise > 10 mmol/day
  • creatinine rate of rise >100micromol/day

To maintain good calcium phosphate homeostasis:

  • Dietary phosphate intake should be limited in patients with hyperphosphatemia.
  • Phosphate binding agents are required in the treatment of hyperphosphatemia.
  • For choice of phosphate binder, it is reasonable to take into account the following:
    • Serum calcium,
    • CKD stage,
    • Presence of other components of CKD- MBD,
    • Concomitant therapies
    • Side-effect profile of the drug.

The dose of calcium- based phosphate
binders should be restricted in the presence of arterial calcification and/or adynamic bone disease.

In such instances the use of non
calcium based phosphate binders (e.g.
Sevelamer HCl, lanthanum carbonate etc) could be used.

Hypocalcaemia, is treated with calcium salts and active vitamin D analogues. Calcium intake should however, be restricted in patients with hypercalcemia, soft tissue calcification, low PTH and in patients with adynamic bone disease.

Calcitriol or vitamin D analogs, or
calcimimetics, or a combination of
calcimimetics and calcitriol or vitamin D analogs may be used to lower PTH to two to nine times the upper normal limit for the assay in treated patients.

Parathyroidectomy is indicated when
medical therapy fails.

Dialysis:

The patients could benefit from:

  • Maintenance Haemodialysis (HD) (Twice or Thrice weekly HD),
    Continuous Ambulatory Peritoneal Dialysis (CAPD)
  • Kidney Transplantation.

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