Chronic Care Programme



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Chronic Care Programme

Treatment guidelines

Chronic condition

Chronic Renal Disease and Renal Failure

Consultations protocols

Preferred treating provider

Notes

  • preferred as indicated by option

  • referral protocols apply

Provider

Option/plan

General Practitioner

GMHPP

Gold Options

G1000, G500 and

G200.


Blue Options

B300 and B200.

GMISHPP


Pulmonologist

Gastroenterologist

Neurologist

Physician

Cardiologist

Paediatrician

Surgeon

Urologist

Consultations per annum:

General Practitioner



MILD

MODERATE

SEVERE

Serum creatinine <200 umol/l

Serum creatinine 200-400 umol/l

Serum creatinine >400 umol/l



New and Existing Patients

New and Existing Patients

Not on Dialysis

On Peritoneal dialysis

On Haemo dialysis

1

1

1

1

1

  • Follow-up consultation

1

3

3

3

3

Tariff codes

0183; 0187


Consultations per annum:

See list





New and Existing Patients

New and Existing Patients

Not on Dialysis

On Peritoneal dialysis

On Haemo dialysis

  • Initial consultation

1

1

1

1

1

  • Follow-up consultation

3

7

11

11

25

Tariff codes

0142; 0108


Regular care primary consultation dietician:

Dietician






New and Existing Patients

New and Existing Patients

Not on Dialysis

On Peritoneal dialysis

On Haemo dialysis

  • Initial consultation

1

1

1

1

1

  • Follow-up consultation

0

0

0

0

0

Tariff codes

051


Regular care secondary consultation: dietician

Dietician






New and Existing Patients

New and Existing Patients

Not on Dialysis

On Peritoneal dialysis

On Haemo dialysis

  • Initial consultation

1

1

1

1

1

  • Follow-up consultation

0

0

0

0

0

Tariff codes

053







Peritoneal dialysis per day:

Nurse


New and Existing Patients

New and Existing Patients

Not on Dialysis

On Peritoneal dialysis

On Haemo dialysis

  • Initial consultation

0

0

0

0

0

  • Follow-up consultation

0

0

0

12

0

Tariff codes

092




Investigations protocols

Type

Provider

Maximum investigations per annum

Mild

Moderate

Severe

Tariff

New and Existing Patients

New and Existing Patients

Not on Dialysis

On Peritoneal dialysis

On Haemo dialysis

Blood glucose: quantitative

Pathology GP or Specialist

4057; 4050

1

1

1

1

1


Urine dipstick (per stick, irrespective of number of tests on stick)

GP or Specialist

4188

6

12

16

0

0


Albumin

Pathology

3999

2

4

4

4

12

Total protein

Pathology

4117

1

1

1

1

1

Sodium + potassium + chloride + CO2 + urea

Pathology

Specialsit



4171

6

12

16

12

26

Serum creatinine

Pathology

Specialist



4032

6

12

16

12

26

Serum phosphate

Pathology

Specialist



4109

2

4

4

4

4

Serium calcium (spectrophotometric)

Pathology

4017

2

4

4

4

4

Creatinine clearance

Pathology

4223

1

1

1

0

0

24 hour protein

Pathology

4213

1

1

1

0

0

Microalbuminuria: thin layer of chromatography on way

Pathology


4265

4

4

4

0

0


Urine protein (quantitative)

Pathology

4213

4

4

4

0

0

Urine creatinine

Pathology

4221

4

4

4

0

0

FBC

Pathology

Specialist



3755

1

3

4

4

12

Serum Fe

Pathology

4071

0

1

1

2

4

Iron binding capacity

Pathology

4073

0

1

1

2

4

Ferritin

Pathology

4528

1

1

1

2

4

Serum folate

Pathology

4536

1

1

1

1

1

Parathyroid hormone

Pathology

4512

0

1

1

1

1

Serum magnesium

Pathology

4094

0

0

0

0

3

Serum aluminium

Pathology

4374

0

0

0

0

1

Hepatitis B screen

Pathology

4531

0

0

0

0

4

HIV


GP; Specialist; Pathology

3932

0

0

0

0

4


Renal ultrasound

Radiology Specialist

3628

1

1

1

1

1

CXR

Radiology

3445

1

1

1

1

1

ECG without effort

GP or Specialist

1232

1

1

1

1

1

Haemodialysis (maximum 8 hours)

Specialist

1849

0

0

0

0

156

ICD 10 coding

N18.




General

Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss of renal function over a period of months or years through five stages. Each stage is a progression through an abnormally low and deteriorating glomerular filtration rate, which is usually determined indirectly by the creatinine level in blood serum.[1]

Stage 1 CKD is mildly diminished renal function, with few overt symptoms.



Stage 5 CKD is a severe illness and requires some form of renal replacement therapy (dialysis or renal transplant). Stage 5 CKD is also called end-stage renal disease (ESRD), chronic kidney failure (CKF) or chronic renal failure (CRF). ESRD is how the US Centers for Medicare and Medicaid Services and US federal legislation reference this stage of illness.

Signs and symptoms

Initially it is without specific symptoms and can only be detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

  • blood pressure is increased due to fluid overload and production of vasoactive hormones, increasing one's risk of developing hypertension and/or suffering from congestive heart failure

  • Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Urea is excreted by sweating and crystallizes on skin ("uremic frost").

  • Potassium accumulates in the blood (known as hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias)

  • Erythropoietin synthesis is decreased (potentially leading to anemia, which causes fatigue)

  • Fluid volume overload - symptoms may range from mild edema to life-threatening pulmonary edema

  • Hyperphosphatemia - due to reduced phosphate excretion, associated with hypocalcemia (due to vitamin D3 deficiency).

    • Later this progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular calcification that further impairs cardiac function.

  • Metabolic acidosis, due to decreased excretion of bicarbonate by the kidney. This may cause altered enzyme activity by excess acid acting on enzymes and also increased excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid (acidemia) [2]

People with chronic kidney disease suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with chronic kidney disease and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.




Diagnosis

Suggestive features

In many CKD patients, previous renal disease or other underlying diseases are already known. A small number presents with CKD of unknown cause. In these patients, a cause is occasionally identified retrospectively.

It is important to differentiate CKD from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound is commonly performed, in which the size of the kidneys are measured. Kidneys with CKD are usually smaller (< 9 cm) than normal kidneys with notable exceptions such as in diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CKD and ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests) it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible.

Additional tests may include nuclear medicine MAG3 scan to comfirm blood flows and establish the differential function between the two kidneys. DMSA scans are also used in renal imaging; with both MAG3 and DMSA being used chelated with the radioactive element Technetium-99.

Numerous uremic toxins (see link) are accumulating in chronic renal failure patients treated with standard dialysis. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.


Causes

The most common causes of CKD are diabetic nephropathy, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.

Historically, kidney disease has been classified according to the part of the renal anatomy that is involved, as:



  • Vascular, includes large vessel disease such as bilateral renal artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome and vasculitis

  • Glomerular, comprising a diverse group and subclassified into

    • Primary Glomerular disease such as focal segmental glomerulosclerosis and IgA nephritis

    • Secondary Glomerular disease such as diabetic nephropathy and lupus nephritis

  • Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy

  • Obstructive such as with bilateral kidney stones and diseases of the prostate

Stages of Chronic Kidney Disease

All individuals with a Glomerular filtration rate (GFR) <60 mL/min/1.73 m2 for 3 months are classified as having chronic kidney disease, irrespective of the presence or absence of kidney damage. The rationale for including these individuals is that reduction in kidney function to this level or lower represents loss of half or more of the adult level of normal kidney function, which may be associated with a number of complications [3].

All individuals with kidney damage are classified as having chronic kidney disease, irrespective of the level of GFR. The rationale for including individuals with GFR 60 mL/min/1.73 m2 is that GFR may be sustained at normal or increased levels despite substantial kidney damage and that patients with kidney damage are at increased risk of the two major outcomes of chronic kidney disease: loss of kidney function and development of cardiovascular disease.[4]

Stage 1 CKD

Slightly diminished function; Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2). Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies.[5] [6]

Stage 2 CKD

Mild reduction in GFR (60-89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies.[7]

Stage 3 CKD

Moderate reduction in GFR (30-59 mL/min/1.73 m2) [8]

Stage 4 CKD

Severe reduction in GFR (15-29 mL/min/1.73 m2) [9]

Stage 5 CKD

Established kidney failure (GFR <15 mL/min/1.73 m2, or permanent renal replacement therapy (RRT)[10]



Treatment

The goal of therapy is to slow down or halt the otherwise relentless progression of CKD to stage 5. Control of blood pressure and treatment of the original disease, whenever feasible, are the broad principles of management. Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression of CKD to stage 5.[11][12]
Replacement of erythropoietin and vitamin D3, two hormones processed by the kidney, is usually necessary, as is calcium. Phosphate binders are used to control the serum phosphate levels, which are usually elevated in chronic kidney disease.When one reaches stage 5 CKD, renal replacement therapy is required, in the form of either dialysis or a transplant.

Medicine formularies

Plan or option


Link to appropriate Mediscor formulary

GMHPP

Gold Options G1000, G500 and

G 200

Blue Options B300 and B200



GMISHPP

[Core]

Blue Option 100



n/a

Epidemiology

· Predominant age: All ages¾more common in adults; increasing prevalence and incidence in the elderly

· Predominant sex: Male > Female (3)




Prognosis

The prognosis of patients with chronic kidney disease is guarded as epidemiological data has shown that all cause mortality (the overall death rate) increases as kidney function decreases.[13] The leading cause of death in patients with chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.[13][14][15]

While renal replacement therapies can maintain patients indefinitely and prolong life, the quality of life is severely affected.[16][17] Renal transplantation increases the survival of patients with stage 5 CKD significantly when compared to other therapeutic options;[18][19] however, it is associated with an increased short-term mortality (due to complications of the surgery). Transplantation aside, high intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional thrice weekly hemodialysis and peritoneal dialysis.[20]



References

  1. http://www.kidney.org/professionals/KDOQI/guidelines_ckd/p4_class_g1.htm NKF K/DOQI GUIDELINES

  2. Adrouge HJ, Madias NE. Changes in plasma potassium concentration during acute acid-base disturbances. Am J Med 1981; 71: 456-67

  3. http://www.kidney.org/professionals/KDOQI/guidelines_ckd/p6_comp.htm NKDOQI guideline Part 6 ASSOCIATION OF LEVEL OF GFR WITH COMPLICATIONS IN ADULTS

  4. http://www.kidney.org/professionals/KDOQI/guidelines_ckd/p7_risk.htm Part 7 STRATIFICATION OF RISK FOR PROGRESSION OF KIDNEY DISEASE AND DEVELOPMENT OF CARDIOVASCULAR DISEASE

  5. http://www.kidney.org/professionals/KDOQI/guidelines_ckd/Gif_File/kck_t12.gif NKDOQI guidelines Table 12

  6. Slate, Melissa K., RN, Chronic Renal Failure http://www.rn.org/

  7. http://www.kidney.org/professionals/KDOQI/guidelines_ckd/Gif_File/kck_t12.gif NKDOQI guidelines Table 12

  8. Slate, Melissa K., RN, Chronic Renal Failure (2008) http://www.rn.org/

  9. Slate, Melissa K., RN, Chronic Renal Failure (2008) http://www.rn.org/

  10. Slate, Melissa K., RN, Chronic Renal Failure (2008) http://www.rn.org/

  11. Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet. 1998 Oct 17;352(9136):1252-6. PMID 9788454.

  12. Ruggenenti P, Perna A, Gherardi G, Garini G, Zoccali C, Salvadori M, Scolari F, Schena FP, Remuzzi G. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria. Lancet. 1999 Jul 31;354(9176):359-64. PMID 10437863.

  13. a b Perazella MA, Khan S. Increased mortality in chronic kidney disease: a call to action. Am J Med Sci. 2006 Mar;331(3):150-3. PMID 16538076.

  14. Sarnak MJ, Levey AS, Schoolwerth AC, Coresh J, Culleton B, Hamm LL, McCullough PA, Kasiske BL, Kelepouris E, Klag MJ, Parfrey P, Pfeffer M, Raij L, Spinosa DJ, Wilson PW; American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Circulation. 2003 Oct 28;108(17):2154-69. PMID 14581387. Free Full Text.

  15. Tonelli M, Wiebe N, Culleton B, House A, Rabbat C, Fok M, McAlister F, Garg AX. Chronic Kidney Disease and Mortality Risk: A Systematic Review. J Am Soc Nephrol. 2006 May 31; PMID 16738019.

  16. Heidenheim AP, Kooistra MP, Lindsay RM. Quality of life. Contrib Nephrol. 2004;145:99-105. PMID 15496796.

  17. de Francisco AL, Pinera C. Challenges and future of renal replacement therapy. Hemodial Int. 2006 Jan;10 Suppl 1:S19-23. PMID 16441862.

  18. Groothoff JW. Long-term outcomes of children with end-stage renal disease. Pediatr Nephrol. 2005 Jul;20(7):849-53. Epub 2005 Apr 15. PMID 15834618.

  19. Giri M. Choice of renal replacement therapy in patients with diabetic end stage renal disease. EDTNA ERCA J. 2004 Jul-Sep;30(3):138-42. PMID 15715116.

  20. Pierratos A, McFarlane P, Chan CT. Quotidian dialysis--update 2005. Curr Opin Nephrol Hypertens. 2005 Mar;14(2):119-24. PMID 15687837


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