Both kidneys are located along the rear wall of the abdomen, outside the peritoneal cavity. In the adult human kidney weight was about 150 each it's about as big fist. On the medial side of each kidney Depression, which is called (in Latin) hilus. Passes through the renal hilum the arteries, veins, lymph vessels, nerves and ureter.
Whether the kidney is cut from top to bottom, one can see two main areas: the outer part called the cortex (lat. cortex), and the inner part called the core (Lat. medulla). The core is divided into a number of conical shape formation, called renal pyramids. Each pyramid starts with the base, which is located on the border imeđu cortex and medulla, and ends as the nipples (Lat. papilla), which protrudes into the space pelvis (Lat. pelvis renales), funnel continuation of the upper end of the urethra (lat. ureter).
The nephron is the basic functional unit of the kidney and consists of two main parts:
First glomerulus (glomerular capillaries) through which a large amount of fluid filtered from the blood and
Second long tubule in which the way to the renal pelvis, the fluid filtered into the urine.
Each human kidney contains approximately one million nephrons, each nephron is able to produce urine. The kidney can re-create (regenerate) new nephrons. Because their numbers are gradually decreasing due to renal injury, illness or due to aging. After the 40th age number of functional nephrons prilbližno usually decreases 10% every ten years. This reduction does not endanger life, because adaptive changes in other nephron allow drainage of the required amount of water, electrolytes and waste products.
The creation of urine has four basic phases:
First renal artery after multiple branching blood to glomeruli
Second occurs in the glomerular ultrafiltrate of plasma that enters the system Bowmanovu capsule and drainage canals
Third tubules in the process of changing the filtrate reabsorption and secretion
4th final urine flows into the pelvis and the left kidney through the ureter, urinary bladder and urethra.
Pathophysiology:
Kidney disease may therefore be due to disorders that primarily affect the blood vessels, glomeruli, tubules and interstitial tissue that separates individual nephrons.
In addition to the kidney disease, renal function may be disturbed and the effects izvanbubrežnih factors. Different prerenal factors may reduce renal perfusion so much blood that lead to secondary disturbances in kidney function. Similarly renal disease can occur and the effects postrenalnih factors that lead to blockage of drainage of the urinary tract
Acute renal failure:
Acute renal failure is a clinical syndrome characterized by deterioration of renal function impairment in the excretion of water, electrolytes, hydrogen ions, the decay products of protein metabolism. This syndrome is now generally seen in the syndrome of multiple organ failure. Only about 8% of acute renal failure occurs as an isolated problem. Size diuresis in the clinical syndrome of acute renal failure is uncertain indication and 30% of cases diuresis remains held, otherwise the development of oliguria (urine output <500 ml urina/24h) or anuria (urine output <100 ml/24h). Since 2/3 of acute azotemia throughout the world result prerenal uremia most important measure in this state for the timely correction of insufficient circulating volume. In ca 25% for the uremia of renal lesions.
The transition from acute to chronic renal failure, is not that common and occurs in approximately 9% of cases.
Chronic renal failure:
Chronic renal failure is a clinical syndrome that indicates a progressive and continuous deterioration of the nephron leading to failure of renal function:
First excretory (water, elektoliti, degradation products of protein metabolism)
Second endocrine (secretion of erythropoietin, vitamin D3, vasodilator prostaglandins)
Third metabolic (biologically important substances, drugs, ..)
Chronic renal disease is kidney damage or a reduction in renal function, ie. glomerular filtration rate less than 60 mL/min/1.73 m2 for more than three months. Renal means abnormal urine, biochemical blood tests, x-ray findings or other imaging and renal biopsy.
The main criterion for determining the stages of chronic kidney disease and reduce the size of the glomerular filtration rate. We distinguish five stages:
Stage I - patients with a glomerular filtration (GF)> 90 ml/min/1.73m2 but kidney damage (eg proteinuria)
Stage II - patients with GF 60-89 ml/min/1.73m2
Stage III - patients with GF 30-59 ml/min/1.73m2
Stage IV - patients with GF 15-29 ml/min/1.73m2
Stage V - GF patients with less than 15 ml/min/1.73m2 or already on dialysis.
In terminal renal failure, ie. uremia kliničkig disorder occurs in numerous organ systems and are presented in Table
TREATMENT:
Dialysis:
On the question of when to start dialysis treatment is not easy to answer. In making decisions we must next levels of biochemical parameters (serum urea, creatinine, electrolytes, hydrogen ions, bicarbonate, ..) to take into account patient age, constitution and comorbidities: diabetes, atherosclerosis, hypertension, cardiomyopathy, anemia, ...) .
If we decide need for hemodialysis vascular access is achieved. As a permanent vascular access should certainly be preferred subcutaneous artrio-venous fistula. It is accepted that it is desirable, especially in people with atherosclerosis, but expressed surgery on the forearm blood vessels and do a few months before the start of hemodialysis.
In this method of treatment we choose the surface of the membrane and the filter coefficient ultrafiltracijski and composition of the dialysis solution.
If we are in agreement with the patient (which we presented to his required training), opted for peritoneal dialysis is necessary to incorporate into the abdominal cavity of the catheter. Then I made dialysis patients (the post-education), at home, loading and unloading into the abdominal cavity to separate the liquid and usually 4x per day. Some authors prefer this method in patients where vascular access is difficult and certainly those who are able to do themselves (capable of education, the space at home, ...). The advantage of this method depends on ostatnoj Ťkvalitetiť diuresis and peritoneal membrane.
Possible complications:
In addition to replacement of renal dialysis treatment is carried out and the many complications that are common and serious complication of a worsening another. That as anemia, hypertension, disorders of calcium and phosphorus metabolism, dyslipidemia, heart failure, etc..
Anemia:
Symptoms in patients with anemia depend on the duration and severity of anemia and signs of underlying disease. Since the symptoms are present kardiorespiratornih hyperkinetic state with palpitations, tachycardia, dyspnea, work, and in case of reduced myocardial reserve are possible symptoms of heart failure. Neuromuscular symptoms include headaches, dizziness, weakness, fatigue, tinnitus, cramps in the calves, increased sensitivity to cold, and the like. . Of gastrointestinal symptoms reported a loss of appetite, nausea, diarrhea and constipation. Genitourinary symptoms include menstrual disorders, loss of libido, frequent urination.
Among the major compensatory mechanisms to anemia belongs to the oxyhemoglobin dissociation curve shift to the right, the redistribution of blood flow, and other compensatory changes in the cardiovascular system and the creation of enhanced erythropoietin. What mechanism will be activated more strongly depends on the cause of anemia, and the speed at which it develops. If you move the oxyhemoglobin dissociation curve to the right, reduce the affinity of hemoglobin for oxygen. Of the factors that shift the oxyhemoglobin dissociation curve to the right of anemia is the most important 2.3-difosfoglicerat (DPG), whose concentration in blood increases during hypoxia. Redistribution of blood provides the key bodies to hypoxia are better supplied with blood from other organs. This was particularly true in the bloodstream to the brain and the coronary circulation where hypoxia causes vazodilaciju, unlike blood flow in the skin and kidneys where the predominant vasoconstriction caused by sympathetic stimulation.
Compensatory mechanisms which I have so far said they can not increase the total number of red blood cells or the total amount of hemoglobin in the body. Therefore, it is clear that these mechanisms can not completely normalize the initial disturbance in anemia - a shortage of hemoglobin.
However, the activation mechanism eritropoetinskog bone marrow will start producing red cells increased, erythropoietin will therefore be able to completely compensate for the anemia that are not too serious and that is the cause of the malfunction of the bone marrow.
Anemia in chronic renal failure:
Anemia is one of the most important and frequent complication in chronic renal failure. Clinically, it is typically manifested as early as II. stage and worsens with progression of renal failure.
Morphological characteristics of red blood cells are normokromnost normocitnost and a serum iron, transferrin levels, serum ferritin and transferrin saturation is usually normal. In inflammatory conditions, there was an decrease in serum iron and transferrin, and ferritin increases.
The three main pathophysiological mechanism of anemia in chronic renal failure:
First Inadequate erythropoietin is the primary and most important etiological factor for anemia. Most common is the lack of only relative to the hemoglobin. Hypoxia is a stimulus for the renal secretion of erythropoietin.
Second The presence of inhibitors of erythropoiesis is another important etiologic factor of anemia in chronic renal failure. The bone marrow of these patients showing no compensatory erythropoiesis proliferative response you would expect in anemia.
Third Shortened red cell life and contribute to anemia bleeding tendency, a result of the retention of metabolic products that act much ekstrakorpuskularno causing also platelet dysfunction.
4th Other factors are:
- Lack of important nutrients for erythropoiesis: folic acid, vitamin B12 and iron;
- Aluminum intoxication;
- Hemolysis (acute form occurs. Drugs and chronic form caused by increased activity of spleen
- Dialysis procedure itself leads to loss of blood (still in the system which
Dialysis is a bit of blood left behind because it is impossible to completely rinse).
Treatment of anemia in dialysis patients should be followed as guidelines for the treatment of anemia.Since the expected approval of CIHI erythropoietin to treat anemia in patients with stage assumes the preddijaliznoj is that in these patients led to slowing the progression of renal failure.
Without adequate treatment of anemia all our other measures to prevent and treat cardiovascular complications will be less effective or futile.
How to stop chronic kidney disease?
Today's world is faced with an increase in the number of patients with chronic kidney disease. Because the disease is progressive course it is understandable that an increasing number of patients requiring permanent substitution therapy by dialysis. The increasing number of patients with chronic kidney disease have a significant role of two factors. The first is the aging population and the other, the global epidemic of type 2 diabetes. It is considered that the current number of diabetics to double in the next 20 years.
However, it should be noted that the main cause of mortality in chronic kidney disease patients is progression of renal failure but also cardiovascular disease (CV). This suggests the interconnectedness of the chronic renal disease is a risk factor for CV disease or risk factor is the same progression of chronic kidney disease. In this important role is played by traditional and non traditional risk factors.
Proteinuria:
an important indicator of disease course, ie. The higher the proteinuria to a greater risk of disease progression. Important study (MDRD, REIN) indicate that the reduction of proteinuria to 1 g / d usporuje drop GF for 1-2 ml / min / year. Many studies indicate a protective effect of ACEI in the prevention of progression of renal disease. In patients who can not tolerate ACEI, can be applied angiotensin receptor blockers, whose effect on proteinuria similar. Today there is evidence on the effectiveness of combination ACEI + ARB.
Arterial hypertension:
Chronic kidney disease and hypertension monitored, and the goal of preventing disease progression istivremeno focused on the regulation of blood pressure and proteinuria. The connection is not regulated hypertension and worsening renal function is well-known fact .. Initial treatment consists of ACEI and then different combinations that include a number of the last group of antihypertensive treatment of hypertension guidelines.
Dyslipidemia:
in chronic renal disease is characterized by elevated vrijednsotima LDL-cholesterol and a decreased level of HDL-cholesterol in uremia and in most of the patients, and elevated triglycerides. On the basis of data on the prevention of CV disease is known to decrease LDL-cholesterol by 1 mmol / l for 4-5 years reduces the risk of incident coronary and CV by 25%. It is known that patients on hemodialysis who have high cholesterol have a higher risk of death.
The cause of this paradoxical relationship lies in the severity of disease, malnutrition patients, and signs of systemic inflammation. Obviously this is a high-risk patients, and decreased synthesis of cholesterol is one of the manifestations of an underlying disease.
The benefit of statins is an indisputable fact but it seems that the effect of statins on the prevention of vascular disease of greater clinical significance, but actions on the course of renal disease.
Reduced protein intake:
one of the first recommendations that advise the patient to prevent progression of kidney disease. Meta analysis of five clinical trials showed that a limited protein intake of 0.4 to 0.6 g / kg reduces the risk of renal failure or death by 33%. With reduced protein intake is important to observe other dietary measures, reduced salt intake, regulation of body weight, and avoiding heavy physical exertion.
INSTEAD OF A CONCLUSION:
How much have we learned from the above text and how much we are willing to take it for yourself will depend on how much it will be "young" our heart.
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