Epidemiology of Chronic Renal Failure in Egypt

 

Chronic Renal Failure (CRF)

 

 

CRF can be defined as a chronic reduction of glomerular filtration rate;

 

i.e. a diminution in creatinine clearance and corresponding increase in

 

 serum creatinine.

 

CRF is a complex syndrome consisting of anemia, oesteodystrophy, neuropathy, acidosis and is frequently accompanied by hypertension, susceptibility to infection and generalized deterioration in organ function.⁽⁴⁾

Causes:

In United States as reported by the united states Renal Data System Annual Report the most common disease causing end stage renal disease are diabetes mellitus (30%), hypertension (26%) and glomerulonephritis (14%) however reflux pyelonephritis, renal hypoplasia, dysplasia, congenital cystic disease and renal tumors (Wilms tumor) represent the most prevalent causes.

 

These data should be used either to establish or to exclude the most common causes of CRF in any evaluation of patient with chronic renal failure.⁽⁶⁾

Approach to patient:

In the evaluation of patients with an elevated serum urea and creatinine levels, it is important to establish the following:

1-The acute or chronic nature of the renal function impairment

2-The causes of renal dysfunction.

                                                                                                                                                                                1- 3-The presence of superimposed reversible factor.

 

 

 

 

First, establishing the presence of CRF will influence the long-term survival of the residual renal function second; identification of a specific pathologic process will influence short and long term therapeutic intervention.

 Aggressive treatment of the primary pathologic process as well as the metabolic derangement of CRF will postpone to some extent the progression to ESRD.

Lastly, the identification and correction of any secondary reversible factor contributing to the renal dysfunction may quickly restore a level of renal function compatible with conservative management and will prevent or modify renal damage from a secondary pathologic process.⁽⁶⁾

 

After the presence of CRF is established, the degree of renal dysfunction must be defined in order to guide further intervention. The degree of intervention may range from aggressive treatment of the primary disease and coexisting hypertension in mild renal insufficiency to conservative follow up and preparation of patients for dialysis in those with severe renal insufficiency.⁽⁷⁾

 

 

Monitoring the progression of Chronic Renal Failure:

As the renal function declines, the deteriorated metabolic disorders associated with CRF will result in the following clinical and laboratory manifestations:

Symptoms:⁽⁸⁾

-General:  fatigue, weakness, lethargy.

-Skin:  itching, easy bruising, skin discoloration, pallor or frost

-Cardiovascular: dyspnea, orthopnea, edema or chest pain.

-Gastrointestinal: anorexia, nausea, vomiting, early satiety or hiccups.

-Neuromuscular: decreased ability to concentrate, restlessness, parathesia, muscle cramps and/or twitching.

 

Signs: ^(8,9)

-Skin: pallor, hyperpegmentation, hyperkeratosis and echymosis

-Oral: oral ulcer and uremic breath.

-Cardiovascular:  hypertension with its different grades, ejection systolic murmur, edema, pericardial friction rub.

-Neuromuscular: sensory/motor peripheral neuropathy, drowsiness, mental confusion seizures and may be coma.

 

Laboratory findings:⁽⁶⁾

-Elevated serum urea and creatinine.

-Metabolic acidosis.

-Anemia most commonly normochromic normocytic.

-Proteinuria.

-Granular casts in urine analysis.

Organ dysfunction in CRF:

-Cardiovascular disorder in CRF:

Cardiovascular disease is the primary cause of death in-patient with CRF. The high prevalence of cardiovascular disease exists in CRF because of increased frequency of associated risk factor (Hypertension, lipid abnormalities and diabetes mellitus) in this population.⁽¹⁰⁾

 

-Hypertension in CRF:

          Hypertension occurs in more than 80% of patients with end-stage renal disease. It is either a result of increased cardiac output or increased total peripheral resistance or both. The increase in cardiac output in advanced CRF is predominantly as a result of Na&H2O overload and also a result of anemia, or possibly due to the presence of high flow arterio-venous fistula.⁽¹⁰⁾ The increased peripheral resistance is due to rennin-dependent vassopressor release from the kidneys. So, the most important factors responsible for hypertension in CRF are volume expansion and vasopressor function of the kidneys.⁽¹⁰⁾

 

Ischemic heart disease:

          In the population with end stage renal disease IHD is an important cause of morbidity and mortality. Here risk factors are the following:^(6,10,11)

-Hypertension

-Diabetes mellitus (if it is the cause of CRF).

-Vascular calcification (diabetes –hyperparathyroidism)

 

-Pericarditis:

It is a frequent and serious complication of advanced renal failure with a potential for causing serious arrhythmias, cardiac tamponade and death. Two categories of pericarditis in CRF include:

A-Uremic pericarditis

It is encountered in patients who have ESRD but are not yet on maintenance dialysis therapy.

 

B-Dialysis related pericarditis

In contrast occurs in patients who have advanced CRF and receiving maintenance dialysis.

 

 

-Heart Failure in CRF^(6,11)

Heart failure is a common complication of advanced CRF usually precipitated by increase preload afterload or intrinsic myocardial failure the main causes of heart failure in CRF are

-Neuromuscular abnormalities:

Multiple disturbance of central nervous system function including inability to concentrate, drowsiness and insomnia are among early symptoms of uremia.⁽¹³⁾ Mild behavioral changes, loss of memory and may be associated with neuromuscular irritability including hiccups; cramps, and chorea are common in terminal uremia.⁽¹⁴⁾,

Peripheral neuropathy is common in advanced CRF.

-Gastrointestinal disorders:

GIT disorder in CRF can be divided into two categories either functional disorder or specific anatomic lesions.

A-Functional GIT disorders:

The most common manifestation of GIT symptoms are: anorexia, early morning nausea, vomiting, hiccups, change in taste sensation as renal function deteriorates to end stage. Dyspepsia here may be due to ingestion of iron supplements, Calcium carbonate or aluminum salt, to metabolic acidosis or to primary gastrointestinal pathology as peptic ulcer or diabetic gasteroparesis.

-Bone diseases:

These diseases in dialysis patients are due to the effect of secondary hyperparathyroidism.⁽¹⁷⁾ Hyperparathyroidism appears in many patients when glomerular filtration rate GFR is still in the range of 20-40ml/min. The immediate causes of it over hypocalcaemia and diminished circulating calcitriol levels due to reduction of hydroxylation of 25hydroxycholecalciferol to 1,25dihydrocholecalciferol in the kidney. Hyperparathyroidism is not present in all dialysis patients. In dialysis patients exposed to aluminium, toxic effects on bone can occur either singly or superimposed on hyperparathyroidism.⁽¹⁸⁾

 

-Immunity in Renal Failure:

Most patients with CRF develop serious infections during the course of their disease. Theoretically it is assumed susceptibility to infection can be due to deranged or deficient humoral or cellular immunity, impaired inflammatory reaction or increased exposure to pathogenic bacteria and viruses.⁽¹⁹⁾ Skin tests if done may show impairment of delayed hypersensitivity. Patients with CRF may have low lymphocyte count, and their lymphocytes do not respond normally to mitogenic stimuli.⁽²⁰⁾ The neutrophil count is usually normal in CRFand it rises appropriately in response to infection. However, a transient decrease may occur following dialysis.

-The syndrome of malnutrition in-patient with renal failure:

        Patient with ESRD display signs and symptoms of wasting and malnutrition.

 

Causes:

Reduced nutritional intake as the symptoms of uremia include anorexia, nausea and vomiting those together with altered taste in general

are common patient complaint although these symptoms are somewhat ameliorated by dialysis therapy, they are not usually completely reversed,

as the haemodialysis procedure itself is associated with nausea and vomiting, possibly related to rapid fluid and electrolyte shifts during the treatment.⁽²⁵⁾ Haemodialysis patient have delayed gastric emptying which may exacerbate the anorexia. Required dietary restriction of sodium, potassium and fluid may also make food less palatable. Also mental depression may contribute to decreased caloric intake.⁽²⁵⁾

Intercurrent illness:

Patient with ESRD also suffer from frequent episodes of intercurrent illness, infection particularly of the vascular access, and peritonitis, pulmonary edema, cardiac arrhythmias and other forms of cardiac disease as well as gastrointestinal disease such as peptic ulcer disease are frequent complication of uremia⁽²⁶⁾ Serious illness in these patients result in metabolic stress that may lead to negative nitrogen balance and adversely affect nutritional state.^(27,28)

Magnitude of the problem

The epidemiology  of end-stage renal disease (ESRD) in Egypt

has never been examined on a national scale. Previous reports

have shown that unknown causes of ESRD in Egypt have reached

33%. Schistosomiasis, which is considered a common cause

of renal failure in Egypt, is the cause of about 30% of chronic renal

failure, most of which is due to obstructive uropathy and a small

percentage is due to schistosomal nephritis

About 15% of patients with hepatosplenic schistosomiasis

develop schistosomal nephritis (immune-mediated

 glomerulonephritis) initiated by the schistosomal antigen and

propagated by IgA  The percentage of diabetic patients in the

dialysis population was 8.4% in 1993.  While data regarding the

 prevalence of hypertensive nephrosclerosis in Egypt are

inadequate, it is reported that one in four Egyptians is or will be

hypertensive.  Chronic interstitial nephritis of unknown etiology is increasing .

 

.

 

The prevalence rate of ESRD in Egypt during 1996 was 225 PMP.

A more accurate calculation of the prevalence of ESRD in Egypt

could have been achieved with a higher response rate to the

questionnaire, which would allow better comparison with other countries.

Most ESRD patients in Egypt are undergoing intermittent

haemodialysis treatment (97.1%), while a minority (2.9%) is

treated by peritoneal dialysis.

Very few renal biopsies were performed for patients before

 reaching ESRD which indicates the need for changing the

 education and training programmes for nephrologists to

 emphasize the need for early detection and management of renal

diseases that may be complicated by renal failure.

The increasing mean age of ESRD patients in Egypt reflects the

 universal trend of dialysis patients living longer due to improving

 health care systems. Better health care can decrease the mortality

rate from diabetes and hypertension, but stops short of preventing

ESRD from these diseases. The mean age of ESRD patients in

 Egypt is lower than that of Latin American countries (50.5 years)

and much lower than that of the USA .

Hypertension is responsible for 28% of cases of ESRD in Egypt.

This high incidence coincides with that reported in the USA, Japan,

 Germany and other European countries Although it has

been stated that one out of four Egyptians is or will be

hypertensive, we believe that this high prevalence can be

attributed to the lack of definite diagnostic criteria of hypertensive

nephrosclerosis in Egypt as well as in other parts of the world, and

that a portion of this group is actually ESRD patients with

 concomitant hypertension Chronic glomerulonephritis was the

second leading cause of ESRD in Egypt (16.6%). ESRD of

unknown etiology was responsible for 16.2% of cases, which is a

 high percentage in comparison with more industrialized countries.

Obstructive uropathy due to urinary schistosomiasis (caused by

Schistosoma haematobium) was responsible for 6.0% of cases of

ESRD. This contradicts previous reports which consider urinary

 schistosomiasis a common cause of obstructive uropathy causing

 renal failure in Egypt (30% of cases) [2]. Schistosomal nephritis

(immune-mediated secondary to hepatosplenic schistosomiasis

caused by S. mansoni) [19-21] was found in 3.6% of cases, and it

 is reported that about 15% of patients with hepatosplenic

schistosomiasis develop immune-mediated glomerulonephritis

initiated by schistosomal antigen and propagated by IgA [3]. One

 explanation for the decreasing prevalence of urinary

schistosomiasis (transmitted via the snail Bulinus truncatus), and

the increasing prevalence of schistosomal nephritis (transmitted

 via the snail Biomphalaria alexandrina) is the redistribution of

snails after the construction of the Aswan High Dam more than 30

 years ago. It is now known that the snail responsible for urinary

schistosomiasis is disappearing from some governorates in upper

Egypt [22]. This snail is being replaced by one responsible for

hepatosplenic schistosomiasis, a fact that has been documented

by thermal infrared measurements of the earth's surface using

satellite imagery [23]. This correlates well with the difference in

prevalence of schistosomiasis in upper and lower Egypt. Lower

 Egypt is known to harbour both types of schistosomiasis, while

 upper Egypt used to harbour mainly S. haematobium. The

prevalence in lower Egypt was 6.6% for schistosomal obstructive

uropathy and 6.3% for schistosomal nephritis. The prevalence in

upper Egypt was 8.8% for schistosomal obstructive uropathy and

5.5% for schistosomal nephritis.

For the treatment of anaemia, 46.3% of patients had received a

blood transfusion, while 15.7% had received erythropoietin. The

small number of patients receiving erythropoietin is due to its high

 cost. HBsAg was positive in 4.8% of the patients and did not

 correlate with the blood transfusion. On the other hand, HCV

antibodies were positive in 49.1% of the cases and correlated

significantly with blood transfusions (P < 0.05). The high

percentage of HCV-positive patients in relation to the low

percentage of HBsAg-positive patients is due to the rigid screening

of blood donors for HBsAg for many years, whereas HCV

screening of blood donors has only recently been introduced. The

high prevalence of HCV antibodies has drawn attention to the

need for better control of blood screening and the need to increase

iron and erythropoietin among dialysis patients instead of blood

transfusions.

The rate of renal transplantation was 32 per 1000 dialysis patients

per year in which all kidneys came from living donors. This rate is

 much lower than northern Europe (135 per 1000 dialysis patients)

The low transplantation rate is due to a shortage in the number of

specialized transplantation centres and the lack of cadaveric organ

transplantation. Attempts to establish a programme for cadaveric

organ transplantation are on-going although facing some

obstacles.

The number of deaths among ESRD patients in 1996 was 117 per

1000 dialysis patients. This number is lower than west Asia,

 eastern Europe, north Africa and western Europe, but higher than

northern and southern Europe In order to accurately calculate

 the mortality rate, follow-up surveys over the coming years are

needed. Cardiovascular diseases were the leading cause of death

 (47.0%), followed by cerebrovascular accidents (17.0%). Liver cell

failure accounted for 16.1% of deaths. This high rate can be

attributed to hepatosplenic schistosomiasis and the high incidence

 of hepatic co-morbid conditions such as hepatitis viruses. Age and

co-morbid factors for those who died could not be analysed.

 

When chronic kidney disease is detected, an attempt should be made to

identify and treat the specific underlying condition(s). The guidelines

define major treatment goals for all patients with chronic kidney disease.

These goals include slowing disease progression, detecting and treating

complications, and managing cardiovascular risk factors. Primary care

physicians have an important role in detecting chronic kidney disease

early, in instituting measures to slow disease progression, and in

providing timely referral to a nephrologist

 

Early treatment of chronic kidney disease and its complications may

delay or prevent the development of end-stage renal disease.

Consequently, detection of chronic kidney disease should be a priority for

family physicians

 

Screening patients at risk for chronic kidney disease relies on the

detection of functional abnormalities using readily available, inexpensive

laboratory tests. The measured serum creatinine level is used to calculate

an estimated glomerular filtration rate (GFR). Screening for proteinuria

often alerts the physician to the presence of chronic kidney disease before

changes in the GFR become apparent.

 

Current guidelines recommend screening for kidney disease with a serum

creatinine measurement for use in GFR estimation and analysis of a

random urine sample for albuminuria. Significant kidney disease can

present with decreased GFR or proteinuria, or both. An analysis7 of data

from the third National Health and Nutrition Examination Survey

(NHANES III) showed that 20 percent of persons with diabetes, and 43

percent of persons with hypertension and a GFR below 30 mL per minute

per 1.73 m2, had no proteinuria. Therefore, an estimate of the GFR and a

screening method for proteinuria are required.1

 

Three interventions have been proved to slow the progression of kidney

disease: blood pressure control glycemic control in patients with

diabetes, and reduction of proteinuria with an ACE inhibitor or

ARB. Other interventions that may be beneficial include

lipid-lowering measures, partial correction of anemia,1 and limiting

dietary protein intake to 0.60 to 0.75 g per kg of body weight per day in

patients with a GFR below 25 mL per minute per 1.73 m2.33