|1||Regulation of the water and electrolyte balance in the bodily fluids and concentration of Na+, K+, Cl-, HCO3-, PO43-, Ca2+, glucose, amino acids, uric acid, and urea via filter, absorption, secretion and excretion processes|
|2||Maintaining the base acid balance (absorption of HCO3 – and excretion of H+)|
|3||Regulation of the volume of bodily fluids, excretion of urine (excretion of endogenic and exogenic catabolites)|
|4||Endocrine functions via excretion of renin (pressure control), erythropoetin (maturing of the red blood cells), prostaglandin, synthesis of 1.25 dihydroxycholecalciferol (vitamin D)|
|5||Involvement in the carbohydrate balance (gluconeogenesis)|
Depending on the severity, chronic kidney disease (CKD) can be classified in five stages. The following model, proposed in 2002 by the Kidney Disease Outcome Quality Initiative (K/DOQI), is recognised worldwide.
CHRONIC KIDNEY DISEASE
|Stage||Glomerular filtration rate (GFR)||Description||Creatinine clearance|
|I conservative kidney function||>90 ml/min/1.73 m²||Kidney damage with normal or increased GFR||80–120
|II mild CKD||60–89
|Retention values in general still normal, hypertension and initial secondary hyperparathyroidism possible||60–80
|III moderate CKD||30–59
|Stable increase in the retention values in general without uraemic symptoms, development of renal anaemia, secondary hyperparathyroidism and metabolic acidosis||30–60
|IV severe CKD||15–29
|Development of uraemia symptoms, creatinine in general frequently > 6 mg/dl with conservative treatment temporary stabilisation still possible||13–30
|V terminal CKD||<15-dialysis||Severe uraemic symptoms in general at the latest with GFR < 10 ml/min/1.73 m2, kidney replacement therapy (dialysis or kidney transplant) life-sustaining||<10 ml/min|
The increasing prevalence and incidence of CKD (chronic kidney disease) is a worldwide health problem. In many countries, the incidence is around 200 cases per million inhabitants, whereby the most common cause is diabetes mellitus and this affects at least 40% of new patients.
It is hard to estimate the prevalence and incidence of the early stages of chronic kidney diseases. Data from the USA from 1999 to 2006 reports that 11.5% of Americans are affected. The increasing prevalence can particularly be attributed to an ageing population and partially also to the growing prevalence of diabetes mellitus and hypertension.
The average European incidence of terminal kidney disease (stage V) is around 135 cases per million inhabitants.
The prevalence of CKD, in particular in the early stages, is not precisely known. This also applies for stage III, in which cardiovascular conditions and other complications, such as renal anaemia and osteopathy, usually occur. In general it can be said that chronic kidney diseases and kidney failure are currently under-diagnosed around the world.
Chronic kidney disease is usually associated with age, diabetes mellitus, hypertension, obesity, cardiovascular conditions, diabetic glomerulosclerosis, glomerulonephritis and hypertensive nephropathy.
Diabetes mellitus and arterial hypertension are the most common risk factors for the occurrence of CKD. For this reason, it is particularly important to monitor kidney function in these patients.
The damage occurs in the area of the small blood vessels (diabetic nephropathy). Diabetic nephropathy can be detected at an early stage through the analysis of the albumin presence in the urine. Proteinuria can subsequently occur and can be identified using a urine test. If the proteinuria exceeds a value of 3.5 g in 24 hours then a 'nephrotic syndrome' may occur.
As an important reason for vascular damage, together with diabetes mellitus and dyslipidaemia it represents the preliminary stage of arteriosclerotic damage. Arterial hypertension affects various organs such as the heart (angina, heart attack), the brain (ischaemia, stroke) and kidneys (arteriosclerotic nephritis). Arteriosclerotic nephritis causes a hardening of the kidney blood vessels, resulting in chronic and progressive kidney disease. In order to slow down the progress of the condition, it is beneficial to keep the pressure values at a rough average of 130/85 mmHg, or for diabetics at roughly 120/80 mmHg.
This is a urinary tract infection. One of the triggering factors is vesicorenal reflux, which may lead to progressive damage to the kidneys.
This is a chronic and progressive hereditary condition, in which the kidneys form cysts and these cause a change to the kidney function. The condition can occur in adults and children; the form seen in adults is less severe and more common. A family case history and ultrasound of the kidneys are useful for diagnostic purposes.
Other congenital and hereditary kidney conditions
Apart from cystic kidneys, there are other congenital and hereditary kidney conditions, such as Alport syndrome. This rare condition involves the combined appearance of signs such as minimal blood loss in the urine, chronic and progressive kidney disease and neurosensory deafness for high sounds.
If the damage is caused by inflammation and affects the renal corpuscles, then we talk of glomerulonephritis. It is assessed via various clinical indicators, and also using laboratory analyses (e.g. blood in the urine - also macroscopically visible identified via urine analysis, arterial hypertension, oedema).
Chronic blockage of the excretion ducts
The blockage of the excretion ducts causes chronic kidney damage, which leads to CKD. Examples of congenital blockage include syndrome of the pyeloureteral junction and ureter constriction or blockage. If these conditions occur on one side, then the healthy kidney compensates for the function of the blocked one. Blockages caused by calcification and ureter blockage are referred to as acquired blockage.
Rarer causes of CKD
Further rarer causes are infections (tuberculosis nephropathy) or medication toxicity (e.g. anti-inflammatories, antibiotics).
Early diagnosis of the first signs of kidney disease (e.g. proteinuria) may make appropriate prevention possible.
The diagnosis provides for initial clinical examination and laboratory testing, followed by an examination of kidney function, in which the glomerular filtration rate (GFR), the creatinaemia and the azotaemia are measured.
The glomerular filtration rate (GFR) stipulates the total volume of the primary urine, which is filtered by all functional nephrons over a particular period. In this way, it is possible to determine the filtration capacity of the kidneys. This is a flow which is measured in millilitres per minute (ml/min).
An important index of the GFR is the creatinine clearance (for this purpose urine is collected for 24 hours and calculations are carried out using the Cockroft-Gault formula). The name clearance refers to the kidneys' ability to clear a particular blood volume of analysed substances (e.g. creatinine) over a particular period of time.
In the case of azotaemia (uraemia), the concentration of the nitrogen (urea) which does not contain protein in the plasma is measured.
In the case of creatinaemia, the creatinine in the plasma is measured. The creatinine is a general indicator of kidney function.
There are reference values for both nitrogen and for creatinine.
In the initial stages, chronic kidney disease (CKD) is usually symptom-free and therefore remains undetected. With restricted kidney function, in the advanced stages uraemic syndrome occurs which is the result of the disrupted excretory and endocrine functions of the kidney. As a result of reduced excretion, there is a retention of toxic metabolic products (e.g. urea). With serum urea concentrations of ≥ 240 mg/dl, it can be anticipated that there will be initial uraemic symptoms. The resulting haematological changes include renal anaemia (usually creatinine values ≥ 3–4 mg/dl) and uraemic bleeding tendency.
From a glomerular filtration rate (GFR) < 10–20 ml/min/1.73 m2 ), there are problems with the water, electrolyte and acid-base balance. The increase in total bodily sodium and water increases arterial hypertension and therefore promotes the occurrence of heart failure. Hyperhydration also leads to an increase in body weight, with subsequent oedema formation.
Hyperkalaemia only occurs from stage V. This is the result of an excessive calcium supply from dietary defects or from medication. In addition, hyperkalaemia is promoted through renal metabolic acidosis, which can be attributed to reduced renal hydrogen and potassium excretion. The clinical symptoms are muscle weakness and muscle pains.
Gastrointestinal problems such as loss of appetite, nausea and vomiting are often early symptoms.
The cause of this is the accumulation of uraemia toxins (breakdown products of protein and purine metabolism).
Hyperphosphataemia, which frequently develops with a GFR < 30 ml/min/1.73 m2, is typical for CKD. With increasing restriction of the GFR, patients develop phosphate retention, which increases the blocking of 1-α-hydroxylase of vitamin D. The hypocalcaemia caused by calcitriol deficiency and hyperphosphataemia is a further stimulus for the occurrence of a secondary hyperparathyroidism, which results in the emergence of renal osteopathy. Its main symptoms are bone pains, spontaneous fractures and muscle weakness.
The first step in CKD treatment is to determine the cause of the condition and to remove this cause.
Some pathologies which cause CKD are triggered by factors that can be identified and remedied, such as obstructive nephropathies due to kidney calcification. If their triggers are removed, this will in fact not lead to an improvement in the patients condition, but it will slow down the development of the disease. Examples of this are nephropathies caused by medication or diabetes mellitus.
Nonetheless, chronic kidney disease is a progressive condition and the damage will progress irrespective of the trigger. If the doctor and patient work together to take all measures to slow down the development of the condition then the progression rhythm will reduce and the patient will achieve not only an extension of the kidney's lifetime, but will also be able to look forward to a very good quality of life.
The treatment of CKD includes the following measures:
|1||General measures to reduce the progression rhythm of the condition, such as a low-protein diet and drugs such as ACE inhibitors or AT1 antagonists (conservative treatment).|
|2||Treatment of complications (excessive fluid, bone alteration, anaemia, metabolic acidosis)|
|3||Preparation for replacement therapy (dialysis or kidney transplant).|
It is recommended that medical check-ups be carried out every 4 months for moderate CKD, every 3 months for severe CKD and every 45 days when the glomerular filtrate falls below 15 ml/min. Due to the lack of controlled studies, the recommendations are based on non-controlled studies.
The following points need to be considered during treatment for chronic kidney disease:
retention of the optimum pressure for nephropathy patients of 130/85 mmHg. If the nephropathy patient is diabetic or has proteinuria, then a lower pressure will be beneficial (120/75 mmHg). For patients over sixty years of age, values can reach around 140/90 mmHg; however it is advisable to try to achieve lower values. In the case of hypertension, suitable medication is used to control and, which proves to be useful due to its properties (e.g. ACE inhibitor), slow down the progression.
anaemia can be balanced out through the use of iron and remedies which promote erythropoiesis. The aim is to keep the haemoglobin between 11 and 12 g/dl in order to improve the patient's quality of life and reduce complications associated with anaemia (left-ventricular hypertrophy, increased tiredness, loss of appetite).
the diet aims to reduce the supply of protein and control acidosis, anaemia and calcium-phosphate metabolism and to reduce azotaemia, phosphataemia and PTH (parathormone). In addition, it helps to slow down the progression of the condition and can be seen as an alternative to the replacement treatment for nephropathy patients over the age of 80 with high comorbidity.
Balancing electrolyte alterations:
typical alterations of CKD include hyperkalaemia (restrict dietary potassium supply), acidosis (restrict dietary sodium supply), hyperphosphataemia and hypocalcaemia (increase dietary calcium supply and reduce phosphate supply, supplement calcium). In stages 4–5, patients who are not undergoing dialysis should use phosphorous chelates that are not based on calcium (sevelamer, lanthanum carbonate). In addition, a vitamin D supplement is beneficial (healthy kidneyscontribute to its formation) in order to avoid severe forms of hyperparathyroidism.
an adjusted diet and medication help to keep cholesterol and triglycerides within the normal range (190 mg/dl for cholesterol, 150 mg/dl for triglyceride).
a healthy lifestyle with regular physical activity, without smoking and with moderate alcohol consumption is of fundamental importance.