HistoryThis section has been translated automatically.
Already in ancient Rome, urinary intoxication leading to death within a few days or weeks was described. Richard Bright was the first to interpret proteinuria as an indication of chronic kidney disease and in 1831 described the increased incidence of alcoholism in the context of glomerulonephritis (Singer 1999).
Abusus of analgesics can lead to a so-called analgesic nephropathy, which, however, does not usually end fatally. The patients show an accumulation of malignant tumours in the area of the urinary tract caused by the abusus. The German nephropathologist Mihatsch was the first to describe this phenomenon in 1980 (Geiger 2003).
In 1945, the Dutchman Willem Kolff performed the first successful dialysis using a so-called "rotating drum kidney" in a patient with acute kidney failure. At her later discharge, the patient showed normal kidney function (Hepp 2017).
DefinitionThis section has been translated automatically.
Chronic kidney failure is now referred to in the International Guidelines as "Chronic Kidney Disease" (CKD) (Herold 2020) and in Germany as "chronic kidney disease" instead of the previous designation "chronic renal insufficiency" (Kuhlmann 2015). CKD is a disease in which the following symptoms persist for a period of > than 3 months:
- Reduction of the eGFR < 60 ml / min / 1.73 m² KOF
- and / or
- signs of kidney damage due to pathological changes in serum, urine, histology or imaging (Herold 2020)
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ClassificationThis section has been translated automatically.
CKD is classified by cause (C = cause), glomerular filtration rate (G) and albuminuria (A) = CGA (Kuhlmann 2015).
According to KDIGO (Kidney disease improving global outcomes) CKD is divided into the following stages:
- Stage G 1:
- there is renal damage with normal renal function
- the GFR ml / min / 1.73 m² KOF is at ≥ 90
- the procedure consists of treatment of concomitant diseases, reduction of cardiovascular risk and further progression
- Stage G 2:
- there is kidney damage with slightly reduced eGFR
- the GFR ml / min / 1.73 m² KOF is between 60 - 89
- the procedure consists - just as in stage 1 - of treating the concomitant diseases, reducing the cardiovascular risk and further progression
- Stage G 3a:
- there is renal damage with moderate reduction of the eGFR
- the GFR ml / min / 1.73 m² KOF is between 45 - 59
- in addition to the above mentioned points, a diagnosis and therapy of complications should be carried out
- Stage G 3b:
- this is also a case of kidney damage with a moderately severe reduction of the eGFR
- the GFR ml / min / 1.73 m² KOF is between 30 - 44
- in addition to the above-mentioned points, the complications should also be diagnosed and treated
- Stage G 4:
- there is a serious reduction in the ECFR
- the GFR ml / min / 1.73 m² KOF is between 15 - 29
- the patient should be prepared for renal replacement therapy
- Stage G 5:
- there is a kidney failure
- the GFR ml / min / 1.73 m² KOF is < 15
- the treatment consists of a renal replacement therapy
The above-mentioned stages are additionally supplemented by the factor of albuminuria (albuminuria is an important parameter for assessing nephron damage [Kasper 2015]):
- A 1: < 30 mg / 24 h
- A 2: 30 - 300 mg / 24 h
- A 3: > 300 mg / 24 h (Herold 2020)
Occurrence/EpidemiologyThis section has been translated automatically.
In Germany, an estimated prevalence of chronic kidney disease is found in up to 10 % of the population over 18 years of age (Weckmann 2019) and albuminuria ≥ 30 mg/dl in about 11.5 % of the population (Herold 2020).
The prevalence of CKD is higher in women than in men (Weckmann 2019).
In Europe, the incidence of CKD is 13.5 / 100,000 inhabitants. Due to the increase in hypertension and diabetes patients, the number of patients with chronic kidney disease is constantly rising.
Currently, about 80,000 patients are treated with hemo- or peritoneal dialysis in Germany and about 23,000 are in aftercare after successful kidney transplantation.
Of the patients with chronic kidney disease, only about 1 % reach the stage of dialysis, as the majority of patients die beforehand from cardiovascular or malignant diseases (Kassumeh 2016).
About 2,500 people receive a kidney transplant each year in Germany. About 30 % of these are living donations (Herold 2020).
EtiopathogenesisThis section has been translated automatically.
The following kidney diseases lead most frequently to CKD:
- vascular hypertensive nephropathy (in 23 %)
- primary glomerulonephritis (at 19%)
- diabetic nephropathy (at 15 %)
- Systemic diseases / autoimmune diseases (at 8 %) such as:
- interstitial nephropathy (at 4 %)
- hereditary kidney disease and others
- Cause unknown (at approx. 20 %) (Herold 2020)
- interstitial kidney diseases (caused by drugs; almost as frequent as vascular nephropathy)
- autosomal dominant cystic kidney (about half as frequent as interstitial kidney disease)
- in rare cases due to an obstructive uropathy (Weckmann 2019)
The figures on the cause vary - depending on the literature - not inconsiderably, among other things because the aetiology differs from continent to continent (Kasper 2015).
PathophysiologyThis section has been translated automatically.
Pathophysiologically, two mechanisms play the main cause of damage:
1. initiation of mechanisms dependent on the particular cause of injury such as:
- Deposition of immune complexes
- abnormalities of renal development
- inflammatory changes
- exposure of toxins (in certain diseases of the renal tubules or interstitium).
2nd: a number of progressive mechanisms such as:
- hypertrophy of the remaining nephrons
- Hyperfiltration of the remaining nephrons (Kasper 2015).
The remaining healthy glomeruli thus attempt maintenance of residual renal function by intraglomerular pressure increase with hyperfiltration. Arterial hypertension, if present, greatly enhances this process. This hyperfiltration is mediated by angiotensin II. Angiotensin II also causes increased production of cytokines and growth hormones, which in turn cause glomerular hypertrophy and hyperplasia. In addition, angiotensin II increases glomerular permeability, resulting in loss of glomerular sieving function. As a consequence, proteinuria develops, which in turn can lead to shrunken kidneys as a direct nephrotoxin via progressive glomerulosclerosis (Herold 2020).
Pathophysiological consequences of CKD are:
Impaired renal secretory function: Retention levels do not increase in serum until > than 60% of functional renal tissue has failed, i.e., glomerulus filtrate is < 50 ml / min. The plasma concentration of both endogenous and exogenous (e.g., drugs) substances thus increases, as does their concentration in primary urine. The concentration capacity of the kidney, on the other hand, decreases. The increasing reduction of nephras results in an excess of solutes in the single nephron, resulting in osmotic diuresis with polyuria, polydipsia, and nocturia (Herold 2020).
Disturbances in water, electrolyte and base balance:
1. sodium: As glomerular filtration decreases, fractional excretion of sodium increases exponentially. Above a glomerular filtration rate of < 10 - 20 ml / min / 173m2 KOF, the adaptive capacity of the kidney is exhausted and there is a retention of salt and water with an increase in extracellular space, which in turn causes hypertension. In some cases, however (e.g., tubulointerstitial nephropathy), tubular dysfunction can lead to salt wasting kidney early on. Therefore, a low-salt diet is not generally indicated in patients with CKD.
2. potassium: The potassium balance, on the other hand, is usually balanced even in advanced CKD because of an increase in intestinal potassium secretion on the one hand and an increase in distal tubular potassium secretion from the solitary epithelium on the other. Only in the terminal stage of CKD does hyperkalemia occur due to:
- Exceeding the secretory capacity with excessive potassium intake and / or acidosis.
- decrease of the secretion capacity in case of oliguria
- the lack of sodium in the distal tube, there is no longer sufficient sodium available to exchange for potassium
3. acid-base balance: as soon as the glomerular filtration rate decreases to < 30 ml / min / 173m2 KOF, metabolic acidosis often develops, because at this point the kidneys are no longer able to eliminate the daily H- ions. Persistent acidosis results in:
- osseous release of calcium
- increasing gastrointestinal symptoms such as loss of appetite, nausea, vomiting, etc.
- increase in protein catabolism
- subjectively perceived dyspnea (Herold 2020)
Impairedblood pressure regulation: Impaired blood pressure regulation includes both hypertension and hypotension.
1. Arterial hypertension: Due to an imbalance between vasodilator systems (such as prostaglandins, NO- system) and the vasopressor systems (such as sympathetic nervous system, RAAS [renin- angiotensin- aldosterone system], endothelin system), pathophysiologically arterial hypertension occurs early. In later stages, however, this results predominantly from volume hypertension. Arterial hypertension occurs in 70%-85% of patients as early as stage 3. In the dialysis stage, it is even up to 90 % of patients with CKD. Therapy resistance is found in one quarter of hypertensive patients.
2. Arterial hypotension: Due to an intravascular volume deficiency (e.g. as a result of therapy with diuretics or as a result of dialysis), arterial hypotension often occurs from stage 4 or 5 (Herold 2020).
Cardiovascular disease: CKD itself represents an independent risk factor for cardiovascular disease. Even in patients not on dialysis, for example, severe left ventricular hypertrophy is already found in about 75%. Cardiovascular mortality is also significantly increased, e.g. 11-fold in stage 3b and 21-fold in stage 4 compared to patients with healthy kidneys. Pathophysiologically, risk factors such as arterial hypertension, diabetes, dyslipidemia, smoking, etc. play a role (Herold 2020).
Neurological disorders: Neurological disorders that may occur in patients with CKD include:
1. uremic encephalopathy: Pathogenetically, this is thought to be neurotoxic damage to the peripheral and central nervous systems caused by accumulation of uremic toxins. Encephalopathy correlates with the severity of renal impairment.
2. dysaquilibrium syndrome: dysaquilibrium syndrome occurs during the initiation of dialysis treatment. It arises pathophysiologically as a result of the osmotic gradient formed between the CNS and plasma during effective dialysis. Symptoms may include: muscle spasms, headache, vomiting, restlessness, confusion, cerebral spasms.
3. Autonomic neuropathy: This may develop due to amyloidosis or diabetes mellitus. Symptom is orthostatic dysregulation (especially hypotension due to dialysis - see renal diseases and skin changes).
4. polyneuropathies: these are predominantly found in patients in the stage of dialysis. There are disturbances of sensitivity and cold sensation as well as dysesthesias.
5. restless legs syndrome: restless legs syndrome occurs in about 20-30% of patients on dialysis. Pathophysiologically, a neurotoxic effect by urine toxins is suspected.
6. Cognitive dysfunction up to dementia: This is predominantly a vascular dementia.
Dermatological diseases (see below kidney diseases and skin changes)
1. Uremic pruritus: Uremic pruritus occurs in about 25%-50% of all hemodialysis patients. Xerosis and hyperpigmentation of the skin are frequently seen, with strongly varying localization. Otherwise, the skin is inconspicuous except for scratch lesions and pruritic prurigo nodularis. Therapeutically, fatty cream can be recommended as a skin care product, UV- B phototherapy can be used, dialysis can be intensified, and pregabalin or gabapentin can be prescribed as off- label. If the patient is transplanted, the symptoms will disappear.
2. Bullous skin lesions: Bullous skin lesions reminiscent of porphyria cutanea tarda (PCT) occur in about 20% of dialysis patients. Patients should avoid excessive exposure to light in that case.
Clinical featuresThis section has been translated automatically.
In the first stages, patients show no or only unspecific symptoms such as:
- performance weakness
- Fatigue (Kuhlmann 2015)
With advanced CKD there are then:
- Respiratory distress (due to pleural or pericardial effusions)
- Loss of appetite
- Lack of concentration
- Bone pain (Kuhlmann 2015)
- Polyneuropathy (mainly affects the sensitive nerves, motor nerves are only affected in severe uremia) (Woolliscroft 2013)
The late symptoms include
- visual disturbances
- uremic gastroenteropathy
- uremic encephalopathy etc. (this clinical picture can hardly be seen in our country nowadays).
DiagnosticsThis section has been translated automatically.
CKD usually develops slowly, over several years. Only after approx. 50% of the functional nephrons have failed, there is an increase in urinary substances in the blood.
Clinical symptoms usually do not exist at this time. Therefore, the diagnosis in the early stages is rather random, e.g. if an increased serum creatinine or a decreased eGFR is noticed during routine examinations (Herold 2020).
- elevated serum creatinine in preliminary examinations
- positive family history of kidney disease
- Taking nephrotoxic drugs such as painkillers, ACE inhibitors, allopurinol, calcium channel blockers, cephalosporins, aminoglycosides, digoxin, methotrexate, penicillamine, loop diuretics, sulfonamides and others [Weckmann 2019])
- diabetes mellitus
- arterial hypertension
- multiple myeloma (Herold 2020)
Inspection and physical examination
- pale grey-brown skin colour (due to anaemia and deposition of urochromes)
- Scratch marks
- Edema (Füußl 2010)
- Blood pressure measurement (Weckmann 2019)
ImagingThis section has been translated automatically.
Sonography: Sonographically the kidneys may be reduced in size with a narrowed parenchymal border. The vessels may show arteriosclerotic changes (Herold 2020)
Echocardiography: Echocardiographically there is often a concentric left heart hypertrophy (Herold 2020)
Diagnosis by x-ray: Routinely, x-rays for the diagnosis of renal osteodystrophy should not be taken, only in case of a well-founded suspicion. This will show:
- subperiosteal erosions mainly on the hand skeleton, but also on the clavicles and the pelvic ring bone
- on the end phalanges of the fingers Acroosteolyses
- on the spinal skeleton, so-called Rugger-jersey marks (band-shaped sclerosing in the area of the base and ceiling plates [Bücheler 2006]) (Kuhlmann 2015)
Kidney biopsy: Usually the nephrologist decides whether a kidney biopsy is necessary. However, the biopsy is not routinely required in the case of CKD (Weckmann 2019).
The damage of the kidneys by an analgesic abusus affects histologically mainly the renal medulla (Geiger 2003).
Bone biopsy: The bone biopsy may reveal evidence of renal osteodystrophy (Lehnert 2014).
LaboratoryThis section has been translated automatically.
- CBC (normochromic, normocytic anemia typical) (Herold 2020).
- Vit. D
- FGF 23 (fibroblast growth factor 23) (Kassumeh 2016)
- Blood glucose determination and if necessary HbA1c- value
- Serum creatinine
- Calculate eGFR
- Transferrin saturation
- Vit. B 12
- Folic acid
- Blood gas analysis (metabolic acidosis only occurs in advanced CKD)
- Potassium (risk of hyperkalemia in advanced CKD)
- Chloride (risk of hyperchloremia, this can occur even in early stages) (Kasper 2015).
Only from stage G 4 onwards should the following values also be determined:
- Serum phosphate determination (often there is hyperphosphatemia)
- Parathormone (possibly elevated)
- Vitamin D (Weckmann 2019)
- Proteinuria (Weckmann 2019)
- Albuminuria (albuminuria is the most important risk factor for progression of CKD and for the development of cardiac risk [Herold 2020])
- Hematuria (Weckmann 2019).
- Protein determination in 24 h urine (Woolliscroft 2013).
Differential diagnosisThis section has been translated automatically.
- Acute renal failure:
- short medical history
- Haemoglobin values normal
- no evidence of renal osteodystrophy
- Kidneys sonographically normal size or enlarged
Complication(s)This section has been translated automatically.
See also under "Pathophysiology": "Pathophysiological consequences of CKD are".
Complications in the course of CKD can lead to the following disorders:
- water and electrolyte balance (mostly occurring from stage 4)
- hyperhydration (usually occurring from stage 4 onwards)
- hyperkalemia (mostly occurring from stage 3 b)
- Acid-base balance (mostly occurring from stage 3 a)
- metabolic acidosis
- Mineral and bone metabolism (mostly occurring from stage 2)
- disturbances of calcium and phosphate balance
- secondary hyperparathyroidism
- renal osteopathies
- blood pressure regulation
- arterial hypertension (mostly occurring from stage 2)
- arterial hypotension (mostly occurring from stage 4 - 5)
- Metabolic disorders (mostly occurring from stage 3 a) in the area of:
- protein metabolism
- carbohydrate metabolism
- Energy-wasting syndrome (protein-energy-wasting syndrome = PEW [Carrero 2016])
uremic gastroenteropathy with
- Nausea (mostly occurring from stage 4 - 5)
- Loss of appetite
- hormonal disturbances
- Immunocompetence disorders
- hematological complications (mostly occurring from stage 3 a)
- thrombopathy with bleeding tendency
- cardiovascular complications (mostly occurring from stage 3 a)
- neurological complications (mostly occurring from stage 3 b):
- cognitive dysfunction up to dementia
- uremic encephalopathy (usually occurring from stage 5)
- dysaquilibrium syndrome (rare but serious complication at the end of hemolysis [Nowack 2009])
- peripheral uremic polyneuropathy
- autonomic neuropathy
- restless legs syndrome
dermatological complications (mostly occurring from stage 3 b - 4)
- joint diseases (Kuhlmann 2015)
TherapyThis section has been translated automatically.
Patients should be presented promptly to a nephrologist for:
- evidence of proteinuria or albuminuria on at least two occasions
- at least two cases of erythrocyturia, micro- or macrohaematuria
- existing CKD with uncontrollable arterial hypertension (despite quadruple medication)
- rapid deterioration of renal function with a drop in GFR of > 5 ml / min / 1.73m3 KOF per year
- morphological changes of the kidney such as sonographically recognizable shrinkage of the kidneys or with different kidney sizes
- presence of anaemia or disturbances of the calcium-phosphate balance with a GFR < 60 ml / min / 1.73m3 KOF
- Initial diagnosis in the existing stage 3 b
- Initial diagnosis in existing stage 3 a and one of the above-mentioned additional criteria
- Patients with impaired renal function and post-myocardial infarction or apoplexy (Wolf 2020)
Albuminuria is the most important risk factor for progression of CKD (Herold 2020).
- Diet: There is little evidence for the specific dietary recommendations sometimes found in the literature. Therefore, dietary recommendations regarding potassium, phosphate, sodium chloride and calories should be based solely on the severity of CKD. From stage G 4 onwards, presentation to a nutritional counsellor is recommended. The evidence regarding the previously generally recommended restriction of protein is contradictory. Meanwhile, only from stage G 4 recommends a reduced protein intake of 0.55-0.6 g / kg bw / d. (Weckmann 2019).
- Fluid: Patients with CKD should consume sufficient fluid in early stages (about 2 l / d). The restriction of the amount of fluid is only when signs of heart failure appear or the patient needs dialysis (Weckmann 2019).
- Nicotine abstinence (Herold 2020)
General therapyThis section has been translated automatically.
Therapy of CKD consists on the one hand of treatment of the underlying disease (if at all possible) and on the other hand of measures to delay further progression (Herold 2020).
Target blood pressure: A target blood pressure of < 140 / 90 mmHg should be aimed for in patients with albuminuria of < 300 mg / dl and absence of diabetes mellitus, and a blood pressure of ≤ 130 / 80 mmHg in patients with albuminuria of > 300 mg / dl. (Herold 2020). Medications that can be considered are: e.g. ACE inhibitors or angiotensin- receptor blockers, but not in combination (this poses a risk of permanent deterioration of renal function, hyperkalemia and arterial hypotension).
Worsening of eGFR (25% of baseline is acceptable) and serum creatinine (30% of baseline is considered acceptable) occurs with treatment. If the limits are exceeded, a dose reduction should be made or the drug should be discontinued. Patients with arterial hypertension should not exceed the recommended 6 g of saline (Weckmann 2019).
Diabetes mellitus: The HbA1c- target value is 6.5 - 7.5 %. The oral antidiabetic drug glibenclamide is contraindicated. Other oral antidiabetic drugs should be adapted to the stage of CKD, such as:
- Empagliflozin: 10 mg / d until eGFR of > 45 ml / min / 173m2 KOF, then contraindicated.
- Glimepiride: 1 - 6 mg / d, reduce from stage G 3.
- Metformin: 500 - 2250 mg / d, from stage G 3 reduce to a maximum of 2 x 500 mg / d, then contraindicated
- Sitagliptin: 100 mg / d, from stage G 3 reduction to 50 mg / d, from stage G 4 to 25 mg / d
Do not need to be adjusted:
- Gliquidon 30 - 90 mg / d
- Insulins (Weckmann 2019)
Cardiovascular management: Since patients with CKD have an increased risk of cardiovascular events and this increases during the course of CKD, cardiovascular risk should be determined early by validated risk calculators. These include:
1. - PROCAM- Risk calculator (PRospektiven CArdiovaskulären Münsterstudie) (www.cmd-taskforce.org/risk-assessment/).
This is used to make statements about the probability of fatal and non-fatal cardiovascular events. Evaluation of the test:
- A high risk exists with multiple risk factors. Here, the 10-year risk for lethal and non-lethal events is > 20%.
- An intermediate risk is present with 2 risk factors. The 10-year risk for lethal and non-lethal events is 10 % - 20 %.
- A low to moderate risk is present with 1 risk factor. Here, the 10-year risk for lethal and non-lethal events is < 10% (Herold 2020).
2nd - ESC- Risk Calculator- Score(www.scores.bnk.de/esc.html): With this score, statements can be made about the probability of fatal cardiovascular events. A very high risk of fatal cardiovascular events of ≥ 10% exists with:
- documented cardiovascular disease, such as: myocardial infarction, cerebral insult, acute coronary syndrome (ACS), coronary arterial bypass grafting (CABG); peripheral arterial disease (PAVD)
- Existing diabetes mellitus with ≥ 1 risk factor and / or end-organ damage.
- severe chronic renal dysfunction with an eGFR: < 30 ml / min / 1.73m3 KOF.
- A high risk of fatal cardiovascular events of 5% - 10% is associated with:
- diabetes mellitus without risk factors and without end-organ damage
- Moderate chronic renal dysfunction with an eGFR between 30 - 59 ml / min / 1.73m3 KOF.
- A moderate risk of fatal cardiovascular events is 1% - 5%.
- A low risk of fatal cardiovascular events is < 1% (Herold 2020).
Reduction of proteinuria: Proteinuria can be reduced by 30-45% with the administration of an ACE inhibitor or angiotensin receptor blocker (ARB), provided the drugs are dosed out (Herold 2020). See also "Therapy" under "Nutrition."
Metabolic acidosis. In metabolic acidosis, the serum bicarbonate concentration drops < 22 mmol / l. Metabolic acidosis can occur in CKD as early as stage G 3 a and occurs in > 90% of patients at stage G 5 (Kuhlmann 2015). Therapeutically, patients should initially increase their intake of fruits and vegetables by dietary means when acidosis occurs. Medication should be used to treat acidosis when:
- tendency to hyperkalemia
- secondary hyperparathyroidism
should be treated with e.g. 1 - 2 g / d bicarbonate orally. Bicarbonate levels of > 22 mmol / l should be aimed for, and overcorrection of ≥ 27 mmol / l should be avoided (Kaufmann 2015).
Hypercholesterolemia: In patients with CKD and increased cardiovascular risk, statins should be started early if additional hypercholesterolemia is present, as they reduce the risk of severe cardiovascular risks by about 20% (Weckmann 2019). Meanwhile, treatment with statins is already recommended for patients > 50 years of age and proven CKD from stage G 1 (Wolf 2020).
Anemia: Depending on clinical symptoms, anemic patients should initially receive oral iron supplementation. Since iron absorption is impaired in later stages of CKD, a switch to parenteral substitution is recommended. Regarding transfusion of blood products, one should be cautious in patients for whom transplantation is considered as a treatment option, as transfusion may result in alloimmunization against donor antigens (Weckmann 2019).
Hyperuricemia: Depending on the stage, hyperuricemia frequently occurs in CKD. The cause for this is unclear so far. For asymptomatic hyperuricemia, drug lowering of uric acid is not recommended in stages 1 - 3. If symptoms occur, drug treatment adapted to renal function should be given, e.g. with allopurinol.
- 100 mg / d for an eGFR < 10 ml / min / 1.73 m 2 KOF.
- 200 mg / d for an eGFR of 10 - 20 ml / min / 1.73 m 2 KOF and above.
- Standard dosage (usually 300 mg) with an eGFR > 20 ml / min / 1.73 m 2 KOF
In the acute episode, 3 - 5 days of treatment with prednisolone 30 mg / d has been shown to reduce inflammation. Pain should be treated with paracetamol or metamizole (Weckmann 2019).
Hyperkalemia: Hyperkalemia may occur due to decreased renal clearance (Weckmann 2019). In that case, patients should consume a low-potassium diet (low-potassium foods include canned vegetables, frozen vegetables, sugar, cooked potatoes, white flour products, fats, coffee, tea ect. [Lückerath 2014]). Medication wise, potassium sparing diuretics are contraindicated, as well as medications that affect serum potassium should be avoided such as RAAS inhibitors, NSAIDs (Kasper 2015), ACE inhibitors, and cotrimoxazole. (Herold 2020)
Hyperphosphatemia: Hyperphosphatemia may occur even in earlier stages of CKD. According to studies, there is an association between hyperphosphatemia and increased cardiovascular mortality. S. a. "Bone metabolism" w. u. (Kasper 2015).
Bone metabolism: Alterations in bone metabolism and calcium- phosphate balance are referred to as CKD- MBD. These occur in early stages of CKD, but are usually asymptomatic initially. The following changes are in need of therapy:
- Vitamin D deficiency
- Secondary hyperparathyroidism (Weckmann 2019).
With regard to osteoporosis, biphosphonates can only be given if the eGFR is too 30 ml / min / 173m2 KOF (dosage recommendation: e.g. alendronate 70 mg 1 x per week p. o. [Schubert 2009]). Denosumab is available as an alternative (dosage recommendation: 60 mg s. c. 2 x per year [Kurth 2018]). In case of proven vit. D- deficiency, patients should receive colecalciferol or ergocalciferol (daily requirement: 200 I. E. / d [Siegenthaler 2006]).
Diuretics: As soon as the kidney loses the ability to excrete sodium (this can occur even in early stages), the retention of sodium can lead to an increase in the amount of extracellular fluid. Both of these factors favor the development of:
- peripheral edema
- arterial hypertension
- cardiac insufficiency
The administration of diuretics has a positive effect on the salt balance and counteracts volume overload. Medications that may be considered include:
- Furosemide usual dose 20 - 80 mg / d, maximum dose in advanced CKD: 500 - 1,000 mg / d
- Thiazides such as HCT, xipamide, etc. should be given in addition to the loop diuretic from an eGFR of < 30 ml / min / 173m2 KOF
- Triamterene, amiloride, and aldosterone antagonists such as spironolactone can be used as inhibitors of sodium reabsorption in the collecting tube in refractory hypertension or edema, respectively, if above-mentioned drugs are not sufficient.
- Triamterene should be taken with special caution above an eGFR of 30 - 60 ml / min / 173m2 KOF and is contraindicated above an eGFR < 30 ml / min / 173m2 KOF
- Amiloride can be given up to an eGFR of 30 - 60 ml / min / 173m2 KOF in the usual dose under close monitoring and is contraindicated above an eGFR < 30 ml / min / 173m2 KOF
- Spironolactone should be reduced (e.g., taken every 2 days) starting at an eGFR of 30 - 60 ml / min / 173m2 KOF. From an eGFR < 30 ml / min / 173m2 KOF, spironolactone is contraindicated. (Weckmann 2019)
- Analgesics: Since many analgesics are nephrotoxic, the patient should be given alternatives such as paracetamol, metamizole, etc. NSAIDs, for example, should be administered only briefly and at low doses starting at a GFR of ≥ 30 ml / min / 173m2 KOF and are contraindicated starting at a GFR of < 30 (Weckmann 2019)
- Drug therapy in CKD
Many drugs contain nephrotoxic substances or, for many, the pharmacokinetics of renally eliminated drugs are altered in the presence of CKD. Nephrotoxic drugs include allopurinol, aminoglycosides, various analgesics, selective COX-2 inhibitors, calcium channel blockers, cephalosporins, digoxin, methotrexate, NSAIDs, penicillamine, loop diuretics, sulfonamides, etc. X-ray contrast media should also be avoided or their administration should be subject to a strict indication.
Contraindicated are drugs such as:
- Pethidine (may cause convulsions).
- Metformin from stage G 4 with an eGFR of <30 ml / min / 173m2 KOF (risk of lactic acidosis)
- Sulfonylureas (there is a risk of hypoglycemia with these)
- Methotrexate (may be myelotoxic)
- Spironolactone (risk of hyperkalemia; see "Diuretics" above)
- Eplerenone (risk of hyperkalemia)
- Gadolinium (may lead to nephrogenic systemic fibrosis)
- Cefepime (may cause CNS disorders)
Renally eliminated drugs: Dose adjustment is required if:
- the eGFR is < 60 ml / min / 173m2 KOF
- the Q0 value of the drug is < 0.5 (the Q0 value is the extrarenal excretion fraction in normal renal function; this value can be found at https://dosing.com or https://www.uni-ulm.de/nephrologie/fkd.html)
For renally eliminated drugs that show altered pharmacokinetics, the general rule is:
- therapy should start with a normal starting dose
- the abstention dose should be adjusted according to the prolonged half-life in the presence of CKD, as the half-life increases with decreasing creatinine clearance (Herold 2020 / Weckmann 2019)
Internal therapyThis section has been translated automatically.
Renal replacement therapy : Renal replacement therapy aims to:
- the elimination of urinary substances (such as urea, creatinine, uremic toxins) and water
- correction of the electrolyte and acid-base balance
- the prevention of complications of CKD (Herold 2020).
There are four different clinical pictures that represent an indication for renal replacement therapy:
- I. Acute kidney injury (AKI) with:
- Increase in serum creatinine > 1.0 mg / dl within 24 h
- hyperuricemia > 12 mg / dl
- Anuria > 12 h after conservative therapy
- Uremic gastroenteropathy with symptoms such as nausea, vomiting, disturbed day-night rhythm, pruritus, uremic encephalopathy, uremic pericarditis, etc.
- Acidosis (Herold 2020)
The initiation of dialysis treatment in acute renal failure is discussed differently. Predominantly, it is recommended to start dialysis treatment as soon as the patient experiences an increase in urea to > 214 mg / dl without clinical signs of recovery (Kasper 2015)
- II. continuous dialysis treatment for terminal CKD with:
- Uremic symptoms such as uremic gastroenteritis with nausea and vomiting, disturbed day-night rhythm, pruritus, uremic encephalopathy, uremic pericarditis, etc.
- hyperhydration with fluid lung / edema
- refractory hypertension
- renal acidosis (pH < 7.2 and base excess < - 10 mmol / l)
- Reduction in glomerular filtration rate (with a GFR < 7 ml / min / 173m2 KOF even in the absence of uremic symptoms; in the case of additional diabetes mellitus or malnutrition earlier)
- hyperkalemia (with serum potassium > 6.5 mmol / l, there is an emergency indication)
- renal anemia (despite adequate substitution of erythropoietin and iron, the Hb is < 8.5 g / dl (Herold 2020).
The start of dialysis treatment is also discussed differently in CKD. It is recommended to determine the optimal start for each patient individually (Kasper 2015)
- III. cardiac-induced hyperhydration (Herold 2020).
- IV. For intoxications with dialyzable or ultrafiltratable toxic substances such as various alcohols, barbiturates, salicylates, bromides, lithium, etc. (Kuhlmann 2015).
Four different methods are available for renal replacement treatment:
- 1. hemodialysis (HD).
- 2. hemofiltration (HF) in the form of
- continuous arteriovenous hemofiltration (CAVH)
- continuous venovenous hemofiltration (CVVH)
- 3. peritoneal dialysis (PD) in the form of
- 4. hemodiafiltration (HDF represents a combination of hemodialysis and hemofiltration) (Kuhlmann 2015).
- To 1. Hemodialysis (HD) The principle of hemodialysis is based on diffusion. In this process, primarily low molecular weight substances up to 25,000 Daltons are eliminated. With up to 80 % - 85 %, HD is the most frequently used procedure in Germany. Hemodialysis is performed via dialysis access (AV fistula or AV vascular interposition for permanent dialysis access or AV catheter for temporary access) for several hours several times a week, usually in dialysis centers, less frequently at home. (Kasper 2015 / Herold 2020 / Kuhlmann 2015 / Bergmann 1993)
- To 2. hemofiltration (HF, CAVH, CVVH) In HF - in contrast to hemodialysis - the dialysis fluid is not passed through a dialyzer, but a hemofiltration solution is injected i. v. several times a week and removed again by pressure gradient in the hemofilter. Hemofiltration is based on convection (Bergmann 1993). In this process, larger molecules can be eliminated . Because of the low effectiveness of < 5 %, pure hemofiltration is rarely used nowadays (Kasper 2015).
- To 3. peritoneal dialysis (PD, APD, CCPD, NIPD, CAPD): In Germany, peritoneal dialysis is used in about 6% of patients requiring dialysis (worldwide in about 10%).(Kasper 2015).
In PD, dialysate is instilled into the abdominal cavity via a PD catheter. The peritoneum provides the semipermeable membrane . PD can be applied as continuous (3 - 5 times per day manually) or as automated peritoneal dialysis (in this case, the dialysis exchange takes place automatically, usually at night) (Kasper 2015).
- Hemodiafiltration (HDF) Hemodiafiltration is used by approximately 15% of patients requiring dialysis in Germany (Kasper 2015). The advantage of HDF is that both low-molecular and medium-molecular substances can be eliminated. It usually takes place several times a week over several hours (Herold 2020).
Operative therapieThis section has been translated automatically.
The surgical treatment of a CKD consists of a kidney transplant (NTX).
The transplantation ability of a patient must be evaluated from a GFR of < 15 ml / min / 173m2 KOF and the patient must be prepared accordingly.
In addition, the patient should also be made aware of the possibility of preemptive transplantation (transplantation before initiation of dialysis treatment) (Kuhlmann 2015).
Indication for kidney transplantation is a:
- terminal CKD
Vaccinations: Preoperatively, patients should have sufficient vaccination protection or have regular booster shots, such as:
- hepatitis B
Postoperatively, no vaccinations should be given in the first 6 months (except flu vaccination) and after that only vaccinations with inactive dead vaccines (live vaccines are contraindicated due to immunosuppression). (Herold 2020)
Donation of corpses: The waiting period for a corpse donation is about 5 - 6 years (Herold 2020).
Living donation: Donors are close relatives or people from the immediate environment of the affected person.
In the case of living donation, there is the possibility of an AB0-incompatible transplant (Herold 2020).
Post-operative:Transplanted patients require post-operative lifelong immunosuppression (Herold 2020).
Progression/forecastThis section has been translated automatically.
The following are particularly responsible for the progression of a CKD:
- Non-influenceable factors such as
- male sex
- higher age
- positive family history
- genetic factors
- Influenceable factors such as
- arterial hypertension
- Tobacco consumption
- Albumin excretion rate
- increased BMI (Wolf 2020)
The forecast is improved by:
- early dialysis
- Kidney transplantation (Woolliscroft 2013)
The classification into the G 1 - G 5 and the A 1 - A 3 stages (see above under "Classification") allows a prognostic statement on the progression of renal failure.
- low risk:
G 1 and A 1
G 2 and A 1
- moderately increased risk:
G 1 and A 2
G 2 and A 2
G 3a and A 1
- high risk:
G 3a and A 1
G 1 and A 2
G 2 and A 2
- very high risk:
G 3a and A 3
G 3b and A 2
G 3b and A 3
G 4 and A 1 - A 3
G 5 and A 1 - A 3 (Kasper 2015)
For patients with end-stage CKD between the ages of 20 and 40 years, a kidney transplantation prolongs their life by approximately 17 years compared to dialysis treatment. The prognosis after NTX is better in patients with living donation than in patients with cadaver donation due to the short ischemic time and the possibly more motivated postoperative compliance. (Herold 2020)
Mortality: Total mortality is increased compared to the general population in patients with a decreased eGFR (Herold 2020), also mortality is increased by the occurrence of a pronounced metabolic acidosis (< 17 mmol / l). In dialysis patients, alkalosis (> 27 mmol HCO3) is associated with increased mortality (Kuhlmann 2015).
The 5-year survival rate is 77 % for cadaver donation and 85% for living donations (Herold 2020).
AftercareThis section has been translated automatically.
Patients with CKD require regular follow-up after diagnosis. This should be monitored in particular:
- weight including nutritional and hydration status
- Blood pressure
- urea - nitrogen
- Serum phosphate
- Serum calcium (iatrogenic hypercalcemia must be avoided at all costs due to nephrotoxicity)
- serum alkaline phosphatase
- Albumin (Woolliscroft 2013)
LiteratureThis section has been translated automatically.
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- Bücheler E et al (2006) Introduction to radiology: diagnostics and interventions. Georg Thieme Publisher 66
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- Geiger H et al (2003) Renal diseases: pathophysiology, diagnostics and therapy. Schattauer publishing house 103
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- Schubert I et al. (2009) Guidelines Group Hesse / PMV Research Group: Family practice guidelines. German Doctors Publishing House Cologne 398
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- Singer M V et al (1999) Alcohol and alcohol-related diseases: Basics - Diagnostics - Therapy. Springer publishing house 383
- Weckmann S et al. (2019) S 3- Guideline Care of patients with chronic non-dialysis-related kidney disease in general practice. AWMF register number: 053 - 048
- Wolf G et al (2020) Elsevier Essentials Nephrology: The most important thing for doctors of all specialties. Urban and Fischer publishing house 77 - 86
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Incoming links (9)Chronic kidney disease; Chronic renal insufficiency; Fabry's disease; Gynecomastia; Immunotactoids and fibrillary glomerulopathy; Renal dysplasia with cysts; Renal replacement treatment; Restless legs syndrome; Thrombosis prophylaxis;
Outgoing links (24)Ace inhibitors; Allopurinol; Aminoglycosides; Analgesics; Arterial hypertension; At1 receptor antagonists; Blood gas analysis; Calcium antagonists; Cephalosporins; Chloride; ... Show all
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