Chronic Kidney Disease

(Chronic renal failure; CKD)

As chronic kidney disease (CKD) is defined as a long lasting progressive deterioration of renal function. The symptoms develop slowly and appear as anorexia, nausea, vomiting, stomatitis, dysgeusia, nocturia, fatigue, fatigue, pruritus, decreased mental alertness, muscle spasms and muscle cramps, water retention, malnutrition, peripheral neuropathy, and seizures. The diagnosis is based on laboratory tests of renal function, sometimes on a renal biopsy. The therapy is aimed primarily against the underlying disease, but also includes fluid and electrolyte balance, erythropoietin in anemia and often dialysis and / or kidney transplant.

As chronic kidney disease (CKD) is defined as a long lasting progressive deterioration of renal function. The symptoms develop slowly and appear as anorexia, nausea, vomiting, stomatitis, dysgeusia, nocturia, fatigue, fatigue, pruritus, decreased mental alertness, muscle spasms and muscle cramps, water retention, malnutrition, peripheral neuropathy, and seizures. The diagnosis is based on laboratory tests of renal function, sometimes on a renal biopsy. The therapy is aimed primarily against the underlying disease, but also includes fluid and electrolyte balance, erythropoietin in anemia and often dialysis and / or kidney transplant. Etiology CHD may result from renal dysfunction of any sort with the appropriate amount (see Table: Main causes of chronic kidney disease). The most common causes in the US and Europe are diabetic nephropathy, followed by hypertensive nephrosclerosis and some primary and secondary Glomerulopathies. Metabolic syndromes associated with hypertension and type 2 diabetes have a strong and growing share of the causes of kidney damage. Main causes of chronic kidney disease cause chronic tubulointerstitial nephropathy examples see Table: Causes of chronic tubulointerstitial nephritis Glomerulopathies focal sclerosing glomerulonephritis Idiopathic glomerulonephritis with crescent formation IgA nephropathy Membranoproliferative glomerulonephritis membranous nephropathy Glomerulopathies in systemic amyloidosis diseases diabetes mellitus Good pasture syndrome granulomatosis with polyangiitis hemolytic uremic syndrome Mixed cryoglobulinemia acute proliferative glomerulonephritis SLE Hereditary nephropathies autosomal dominant interstitial kidney disease (medullary renal disease) hereditary nephritis (Alport syndrome) Nage-patella syndrome Polycystic Kidney Disease Hypertension hypertensive nephrosclerosis Obstructive uropathy Benign prostatic Rear urethral valves retroperitoneal fibrosis ureteral obstruction (congenital, stones, cancer) Vesicoureteral reflux Macrovascular kidney disease (vasculopathy of renal arteries and veins) The renal artery stenosis caused by atherosclerosis or fibromuscular dysplasia. Pathophysiology CKD can be divided roughly into reduced renal functional reserve, renal failure or renal disease. Initially, the renal tissue loses its function, but it occurs only a few anomalies, because the remaining tissue increases its capacity (functional renal adaptation). The loss of 75% of the total renal tissue leads to only a 50% reduction in GFR. The renal impairment interferes with the ability of the kidney to maintain fluid and electrolyte. The changes proceed predictably gone, but there is considerable overlap and individual differences. The ability to urine concentration decreases at an early stage, followed by a decreasing ability, phosphate, acid and potassium excrete. If the kidney failure has progressed (GFR ? 10 mL / min / 1.73 m2), lost the ability to urine dilution, so that the osmolality is usually close to the plasma no longer (300-320 mOsm / kg) and the urine volume variations in fluid intake responding. Creatinine and urea plasma concentrations of creatinine and urea, which are highly dependent on the glomerular filtration, leading to a hyperbolic increase in proportion as the GFR decreased. Initially, only minor changes are observed. If the GFR of less than 10 ml / min / 1.73 m 2 (normal = 100 ml / min / 1.73m2), get the mirrors quickly and are often associated with systemic manifestations (uremia). Urea and creatinine are not main cause for the uremic symptoms. Rather, they are a marker for many other substances that trigger these symptoms (and some of which are not yet determined exactly) .Natrium and water Despite a decreased GFR is the sodium-water balance by increased fractional excretion of sodium and a normal thirst response well maintained. Thus, the plasma sodium concentration is typically normal, and Hypervolaemia is rare, unless the intake of sodium or water is very limited or excessive. may especially in patients with decreasing “cardiac reserve” by sodium and water overcharging heart failure entwickeln.Kalium For substances whose secretion mainly through the distal nephron (eg. as potassium) is controlled, the adaptation usually leads to advanced renal failure with a normal plasma concentration. Potassium-sparing diuretics, ACE inhibitors, beta blockers, NSAIDs, cyclosporine, tacrolimus, trimethoprim / sulfamethoxazole, pentamidine or angiotensin II receptor blockers can mask the plasma potassium levels in patients with less advanced renal insufficiency erhöhen.Kalzium and phosphate may be changes in calcium, phosphate parathyroid hormone (PTH) and vitamin D metabolism and come to renal osteodystrophy. Decreased renal production of calcitriol contributes to hypocalcemia. Decreased renal excretion of phosphate leads to hyperphosphatemia. Secondary hyperparathyroidism is common and can lead to kidney failure before anomalies in calcium or phosphate concentrations. For this reason, the monitoring of PTH in patients with moderate CKD was before hyperphosphatemia occurs, recommended. Renal osteodystrophy (abnormal bone mineralization caused by hyperparathyroidism, calcitriol, increased serum phosphate or low or normal serum calcium) is usually in the form of increased bone metabolism due to hyperparathyroidism (osteitis fibrosa), as well as decreased bone metabolism due to an adynamic bone disease (with increased suppression of parathyroid hormone), or osteomalacia. Calcitriol may osteopenia or osteomalacia führen.pH and bicarbonate are characterized by a moderate acidosis (Plasma-bicarbonate content of 15-20 mmol / l) and anemia. Acidosis caused muscle protein catabolism due to, bone loss due to the Knochenpufferung of acid and progression of Nierenerkrankung.Anämie anemia is characteristic of medium to advanced CKD (? 3). The anemia associated with CKD is normochromic normocytic at a hematocrit of 20-30% (35-40% in patients with polycystic kidney disease). It is usually caused by an insufficient erythropoietin production, which is caused by the reduction of the total renal tissue (Reduced erythropoiesis). Other consequences are iron, folate and vitamin B12 deficiency. Symptoms and discomfort for patients with mild depressed renal reserve are asymptomatic. Even patients with a weak to moderate renal insufficiency may be no symptoms despite increased urea and creatinine. Due to the inability to concentrate the urine, there is often a nocturia. Exhaustion, fatigue, anorexia and decreased mental capacity are often the first manifestations of uremia. With development of a stronger renal failure (eg. As creatinine clearance <10 ml / min in patients without diabetes and <15 ml / min in patients with diabetes) neuromuscular symptoms can occur with coarse muscle twitching, peripheral sensory and motor neuropathy, muscle spasms, hyperreflexia, Restless leg syndrome and seizures (usually as a result of hypertensive or metabolic encephalopathy). It almost always comes to anorexia, nausea, vomiting, weight loss, stomatitis and an unpleasant taste in the mouth. The skin may be yellow-brown. Sometimes after sweating urea crystals on the skin to detect (uremic frost). An itch can be particularly unpleasant. Malnutrition, which leads to a general atrophy, is a prominent feature of chronic uremia. In advanced CKD are usually limited to pericarditis and gastrointestinal ulceration and bleeding. Hypertension occurs with advanced CKD at> 80% of patients and is usually associated with hypervolemia or occasionally the result of activation of the renin-angiotensin-aldosterone system. Heart failure caused by hypertension or coronary heart disease and renal retention of sodium and water can lead to edema. Diagnosis electrolytes, BUN, creatinine, phosphate, calcium, blood count, urinalysis (including Harnsedimentprüfung) sonography Sometimes kidney biopsy from a CKD one goes usually from the increases in serum creatinine. The first diagnostic step is to determine whether renal failure is acute or chronic or whether chronic renal failure has acute deteriorated (for example, by an acute disease, which further restricts the renal function in a patient with CKD – ??see table. Distinctions between acute kidney injury and chronic kidney disease). The cause of renal failure is also determined. Sometimes the determination of the duration of renal failure to determine the cause helps. Sometimes it is easier to determine the cause than the duration, and the determination of the cause helps determine the duration. Distinctions of acute kidney injury and chronic kidney disease findings comment Previously known increases in serum creatinine, the most reliable evidence of CKD renal sonography shows small kidney Usually CKD renal ultrasonography shows normal or enlarged kidneys can be AKI or some forms of CKD (diabetic nephropathy, acute hypertensive nephrosclerosis, PCKD , myeloma, malignant Nephroangiosklerose, rapidly progressive Glomer ulonephritis, infiltrative diseases [eg. As lymphoma, leukemia, amyloidosis], obstruction) oliguria, daily increase in serum creatinine and BUN Probably AKI or AKI CKD superimposed “Eye Band keratopathy” Probably CKD No anemia Probably AKI or CKD due PCKD Severe anemia, hyperphosphatemia and hypocalcemia may CKD but can also be AKI Subperiosteal erosions in the Ra diographie Probably CKD Chronic symptoms or complaints (eg. As fatigue, nausea, itching, nocturia, hypertension) Usually CKD AKI = acute kidney injury; CKD = chronic renal disease; PCKD = polycystic kidney disease. Examination includes urinalysis with examination of urinary sediment, electrolytes, urea nitrogen and creatinine, phosphate, calcium, and blood count. Occasionally specific serological tests are needed to determine the cause. The distinction between acute kidney injury and CKD is most likely facilitated by the history of elevated creatinine level or urine by pathological findings. The findings in urine depend on the underlying disease, but wide (> 3 Leukozytendurchmesser) or especially (refractive) wax cylinders are in advanced kidney failure from any cause frequent. Renal ultrasound is typically the detection of obstructive uropathy, and to distinguish between acute kidney injury and kidney CKD due to the size. With the exception of special situations (see table: main causes of chronic kidney disease) patients with CKD small shrunken kidneys (usually <10 cm in length diameter) with a thin hyperechoic cortex. The bodies of the exact diagnosis is more difficult, the more kidney function reaches values ??approaching the stage of renal disease. The most informative diagnostic measure is the kidney biopsy. but it is not recommended if the kidneys appear small and fibrotic in ultrasound. Classification The staging of CKD is a way to quantify its severity. CKD can be divided into five stages. Step 1: Normal GFR (? 90 ml / min / 1,732) and either persistent albuminuria or known structural or hereditary kidney disease Stage 2: GFR 60-89 ml / min / 1.73 m2 Stage 3: GFR 30-59 ml / min / 1.73 m2 stage 4: GFR 15-29 ml / min / 1.73 m2 stage 5: GFR <15 ml / min / 1.73 m2, the GFR (in ml / min / 1.73 m2), by at CKD formula 186.3 x (serum creatinine) -1154 x age) - 0203 are estimated. In female patients, the result is multiplied by 0,742 and in African American patients with 1.21. In African American women the result by 0.742 × 1.21 (0.898) is multiplied. This calculation is not very accurate for patients who are older and much sitting, are very obese or very thin. Alternatively, the GFR can be estimated using the Cockcroft-Gault formula to approximate the creatinine clearance. This equation tends to overestimate the GFR 10-40%. The "Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula" is more accurate than the MDRD and Cockcroft and Gault formula, in particular in patients with GFR close to the normal values. The CKD-EPI equation leads to fewer false positive results that indicate chronic kidney disease and predicts the results better than the other formulas. Clinical Calculator: estimate the glomerular filtration rate according to the equation of the MDRD Study Clinical Calculator: creatinine clearance (measured) forecast the progression of CKD results in most cases by the extent of Proteinämie. Patients with nephrotic proteinuria (> 3 g / 24 h or urine protein / creatinine ratio> 3) usually have a worse prognosis and develop faster kidney failure. The progress can be taken even if the underlying disorder is not active. h have a urine protein <1.5 g / 24 patients, if any, usually a much slower progression. Hypertension, acidosis, and hyperparathyroidism are also associated with a more rapid progression. Therapeutic control of the underlying disease Possible restriction of protein, phosphate and potassium intake of vitamin D supplements are the treatment of anemia and heart failure doses of all medications adjusted as required dialysis at greatly reduced GFR, uremic symptoms or sometimes when hyperkalemia or heart failure Maintaining lying Natriumbicarbonatspiegels at 23 mmol / l underlying disorders and other factors need to be addressed. In particular, the treatment of hyperglycemia in patients with diabetic nephropathy and the treatment of hypertension in all patients at a significantly slower deterioration in GFR leads. Current guidelines recommend a target blood pressure of <140/90 mmHg, but some authors still recommend about 110 to 130 / <80 mm Hg. ACE inhibitors and angiotensin II receptor antagonists slow down the extent of GFR deterioration in patients with most causes of CKD, especially in proteinuric patients. Increased evidence suggests that - compared to each of the two drugs alone - a combined use of ACE inhibitors and angiotensin II receptor blockers complications increases and does not slow the decline in kidney function, although the combined use more reduced proteinuria. Physical activities should not be restricted, although fatigue and exhaustion often put the patient's ability to play sports, borders. A pruritus in elevated serum phosphate can respond to phosphate binders. If the patient does not respond, the irradiation with UV light can be helpful. Nutrition strict protein restriction kidney disease is controversial. The moderate restriction of protein intake (0.8 g / kg / day) is safe and well tolerated by most patients. Some experts recommend 0.6 g / kg / day for diabetics and> 0.8 g / kg / day for non-diabetics when the GFR 25-55 ml / min / 1.73 m2 or 0.6 g / kg / day, when the GFR / is 13-24 ml / min 1.73 m2. Most Urämiesymptome decrease significantly if protein catabolism and urea formation can be reduced. Carbohydrates and fats are fed enough to support the energy balance and to avoid ketoacidosis. Patients who <0.8 g / kg / day were prescribed should be closely monitored by a dietitian. Since dietary restrictions can reduce the required vitamin intake, patients should take a multivitamin with water-soluble vitamins. The administration of vitamin A and E is not required. Vitamin D in the form of 1,25-dihydroxyvitamin D (calcitriol) or analogs should be given as indicated by the PTH levels. The dose is determined depending on the stage of CKD, PTH concentration and phosphate concentrations (see table: Target values ??for PTH and phosphate in chronic kidney disease). Target values ??for calcium are 8.4 to 9.5 mg / dL (2.10 to 2.37 mmol / l); for the calcium phosphate product <55 mg 2 / DL2. Target values ??for PTH and phosphate in chronic renal disease state of chronic kidney disease PTH (pg / ml) phosphate (mg / dl [mmol / l]) 3 35-70 2,7-4,6 (0,87-1,49) 4 70-110 2,7-4,6 (0,87-1,49) 5 150-300 3,5-5,5 (1,13-1,78) PTH = parathyroid hormone A typical initial dose is calcitriol (or Calcitriolanalog) 0.25 mcg p.o. 1 time / day or 1-4 mcg 2 times / week. In order not to risk that Adynamic bone disease is triggered, the PTH levels should not be normalized. A change in diet can be helpful in hypertriglyceridemia. In patients with hypercholesterolemia statin therapy is effective. Fibric (clofibrate, gemfibrozil) may occur in patients increase the risk of rhabdomyolysis with CKD, especially if at the same time be taken statins, whereas ezetimibe appears to be relatively safe (which reduces cholesterol absorption,). The correction of hypercholesterolemia can Fluid intake will only be limited also for slowing of renal underlying disease and improve coronary risk führen.Flüssigkeits- and electrolyte balance, when the serum sodium concentration is <135 mmol / l or present heart failure or severe edema. Of a sodium restriction to 1.5 g / day particularly benefit patients with edema, heart failure or hypertension. The potassium intake is closely related to the meat, vegetables and fruit consumption, and usually requires no adjustment. However, should foods rich in potassium (especially salt substitutes) are to be shunned. Except for hyporeninemic hypoaldosteronism or potassium-sparing diuretics comes hyperkalemia - to end-stage renal failure if the potassium intake to ? 50 mmol / day must be limited - rare. A slight hyperkalemia (<6 mmol / l) may be treated with potassium reduction and correction of metabolic acidosis. More serious forms of severe hyperkalemia (> 6 mmol / l) requiring emergency treatment. A phosphate restriction to <1 g / day is often sufficient to keep the phosphate levels during the early phase of stages 3 and 4 CKD in the desired range. But in the later stages are often phosphate binders such as calcium salts (acetate or carbonate, but are citrate must be avoided) or calcium-containing phosphate binders (sevelamer) is necessary. No more than 1500 mg / day of elemental calcium should as a binder (2000 mg / day of total calcium, plus supplied calcium binder) are added. Metabolic acidosis should be treated in order to bring serum bicarbonate to normal (> 23 mmol / l) and reverse the muscle atrophy, bone loss, and the progression of CKD or slow. Acidosis can (fruits and vegetables mainly) are corrected with oral sources of alkali, such as sodium bicarbonate or an alkaline ash diet. The dose of sodium bicarbonate 1-2 g p.o. is slowly increased 2 times daily, until the bicarbonate concentration is about 23 mmol / l or prohibit signs of sodium overdose further therapy. If the alkaline diet is followed, serum potassium is monitored, because fruit and vegetables potassium enthalten.Anämie and coagulation disorders anemia is a frequent complication of moderate to advanced CKD (? stage 3) and is treated with -if sparingly erythropoiesis-stimulating agents (ESA) as recombinant human erythropoietin (z. B. epoetin alfa). Due to the risk of cardiovascular complications, including stroke, thrombosis, and death, the lowest dose of this medication is given, which is needed to keep the Hb between 10 and 11 g / dl. Because of the increased iron consumption, the iron bearings must be replenished frequently with parenteral iron at increased erythropoiesis. The levels of iron, iron binding capacity, and ferritin should be monitored closely. The selected transferrin saturation (TSAT) calculated by serum iron divided by the total iron binding capacity and multiplied by 100%, should be> 20%; the desired ferritin in patients who are not on dialysis, is> 100 ng / ml. In a transfusion except in severe anemia (Hb <8 g / dL) should be avoided, or if these symptoms causes. The bleeding tendency in CKD rarely needs treatment. Cryoprecipitates, erythrocyte transfusion, Desmopressin (0.3-0.4 mcg / kg [. 20 mcg max] in 20 ml of an isotonic saline intravenously over 20-30 minutes) or conjugated estrogens (2.5-5 mg po 1-times daily ) can help if needed. The effects of this treatment keep 12-48 h at just the conjugated estrogens are several days wirksam.Herzversagen A symptomatic heart failure is treated with sodium restriction and diuretics. In restriction of left ventricular function, ACE inhibitors and beta-blockers should be given. The addition of digoxin is possible, the dose must however be reduced. Diuretics such as furosemide are usually effective in significantly impaired renal function, but high doses may be needed. A moderate to severe high pressure must be treated to prevent its harmful effects on the heart and kidney function. Patients who do not respond to a sodium restriction (1.5 g / day) should receive diuretics (furosemide, 80 to 240 mg po 2 times a day). Hydrochlorothiazide 12.5 mg (starting dose) - 25 mg (often up to 50 mg) of 1-times p.o. daily or metolazone 5-10 mg p.o. can be added to high-dose therapy with furosemide 1 times or 2 times a day if hypertension or edema are under control. Even with kidney failure, the combination of a thiazide diuretic with a loop diuretic is very potent and should be used with caution in order to avoid a "overdiuresis". Sometimes dialysis may be necessary to control heart failure. If the reduction of extracellular fluid volume does not lower blood pressure, conventional antihypertensive drugs must be given in addition. Azotemia may be increased by such treatment and be necessary to heart failure and / or hypertension to kontrollieren.Medikamente Renal excretion of drugs is often disturbed with kidney failure in patients. Among the drugs that usually require dose adjustment is necessary, include penicillins, cephalosporins, aminoglycosides, fluoroquinolones, vancomycin, and digoxin. Hemodialysis reduced the serum levels of some medicines that should be replaced after hemodialysis. is highly recommended that the doctor finds out about medication dosage in renal failure before he prescribes these very sensitive patient medication. Some matching clues include CKD and Drug Dosing: Information for Providers, Drug dosing consideration in patients with acute and chronic kidney disease-a clinical update from Kidney Disease: Improving Global Outcomes (KDIGO), and Drug Dosing Adjustments in Patients with Chronic Kidney Disease , avoid most experts non-steroidal anti-inflammatory drugs in patients with CKD because they can worsen kidney function Certain medications should be avoided completely in patients with chronic kidney disease. u. a. Nitrofurantoin, metformin and Phenazopyrindin. The MRI contrast agent gadolinium has been associated in some patients with the development of nephrogenic systemic fibrosis; because the risk is particularly high when patients estimated GFR / have <30 ml / min 1.73 m2, gadolinium in these patients should, whenever possible, avoided werden.Dialyse dialysis is usually initiated at the beginning of one of the following: uremic symptoms (eg. as anorexia, nausea, vomiting, weight loss, pericarditis, pleurisy) difficulties in controlling fluid overload, hyperkalemia or acidosis These problems occur usually when the estimated GFR ? 10 mL / min in a patient without diabetes or ? 15 ml / min can be achieved in a patient with diabetes. Patients are the estimated GFR values ??in the vicinity of these values ??should be closely monitored so that these signs and symptoms are detected early. Dialysis is good estimate, so that preparations can be made and the mandatory introduction of a hemodialysis catheter can be avoided. Such preparations usually begin when the patient is in the early to middle stage 4 CKD. The preparation allows time for patient education, selecting the type of dialysis and the timely creation of an arteriovenous fistula or placement of a peritoneal dialysis catheter. (Dialysevorbereitung, Hämodialyse). Tipps und Risiken Mit der Vorbereitung für die Dialyse sollte während des frühen bis mittleren Stadiums 4 der CKD begonnen werden, um ausreichend Zeit für die Aufklärung der Patienten und für die Auswahl der Art der Dialyse und der Katheter zu haben. Transplantationen Steht ein Lebendspender zur Verfügung, ist das Langzeitergebnis besser, wenn der Patient frühzeitig ein Transplantat erhält, möglichst schon vor Beginn der Dialyse. Transplantationskandidaten, die keinen Lebendspender haben, sollten nach Dialysebeginn so früh wie möglich eine Leichennierentransplantation erhalten. Fazit Häufige Ursachen für CKD in den USA sind diabetische Nephropathie (am häufigsten), hypertensive Nephroangiosklerose, Glomerulopathien und metabolisches Syndrom. Zu den Auswirkungen von CKD können Hypokalzämie, Hyperphosphatämie, metabolische Azidose, Anämie, sekundärer Hyperparathyreoidismus und Nierenosteodyst

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