Insuficienta renala cronica

Rinichii asigura trei functii majore: - filtrarea sangelui si producerea urinei pentru eliminarea deseurilor, impiedicand astfel acumularea toxinelor in sange - reglarea concentratiei mineralelor si electrolitilor (sodiu, calciu si potasiu) si cantitatea de lichid din organism - producerea de hormoni care actioneaza asupra altor functii ale corpului, precum reglarea tensiunii arteriale (renina) si producerea de globule rosii (eritropoietina).

Insuficienta renala cronica (IRC) reprezinta diminuarea lenta si progresiva a capacitatii de filtrare a rinichilor. IRC survine de obicei drept complicatie a altei boli sau afectiuni. Spre deosebire de insuficienta renala acuta, IRC se instaleaza progresiv, pe parcursul mai multor ani, pe masura deteriorarii rinichilor. Evolutia este atat de lenta, incat primele simptome apar doar dupa ce boala a determinat consecinte clinice

Insuficienta renala cronica reprezinta etapa finala a bolilor renale bilaterale, în special a glomerulonefritelor cronice, a glomerulonefrozelor si a pielonefritelor cronice, a hipertensiunii arteriale maligne, a obstructiilor cailor urinare.

în mod normal rinichiul are o rezerva functionala care-i permite sa se adapteze unor solicitari crescute. în insuficienta renala, distrugerea nefronilor nu mai permite aceasta adaptare. Prima functie alterata este capacitatea de concentratie. în stadiul initial, rinichiul poate asigura homeostazia mediului intern, adica sa mentina constanta cantitatea de sare, apa, substante azotate si electroliti din organism, ceea ce se realizeaza prin unele mecanisme

In aceasta perioada, poliuria se însoteste de hipostenurie, deci de scaderea capacitatii de concentratie. Odata cu progresarea leziunilor, poliuria devine maxima si scaderea capacitatii de concentratie este foarte severa. Aceasta este faza de izostenurie, când densitatea urinii oscileaza invariabil între 1 010 si 1 011. în ultimul stadiu, insuficienta renala se decompenseaza si apare uremia.

chronic kidney disease as either kidney damage or a decreased kidney glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for 3 or more months. Whatever the underlying etiology, the destruction of renal mass with irreversible sclerosis and loss of nephrons leads to a progressive decline in GFR.

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Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2) Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2) Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m2) Stage 4: Severe reduction in GFR (1529 mL/min/1.73 m2) Stage 5: Kidney failure (GFR <15 mL/min/1.73 m2 or dialysis)

Approximately 1 million nephrons are present in each kidney, each contributing to the total GFR. Regardless of the etiology of renal injury, with progressive destruction of nephrons, the kidney has an innate ability to maintain GFR by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons.

This nephron adaptability allows for continued normal clearance of plasma solutes so that substances such as urea and creatinine start to show significant increases in plasma levels only after total GFR has decreased to 50%, when the renal reserve has been exhausted. The plasma creatinine value will approximately double with a 50% reduction in GFR. A rise in plasma creatinine from a baseline value of 0.6 mg/dL to 1.2 mg/dL in a patient, although still within the reference range, actually represents a loss of 50% of

The residual nephron hyperfiltration and hypertrophy, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive renal dysfunction. This is believed to occur because of increased glomerular capillary pressure, which damages the capillaries and leads initially to focal and segmental glomerulosclerosis and eventually to global glomerulosclerosis. This hypothesis has been based on studies of five-sixths nephrectomized rats, which develop lesions that are identical to those

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Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following: Systemic hypertension Acute insults from nephrotoxins or decreased perfusion Proteinuria Increased renal ammoniagenesis with interstitial injury Hyperlipidemia Hyperphosphatemia with calcium phosphate deposition Decreased levels of nitrous oxide Smoking

CKD can be roughly categorized as diminished renal reserve, renal insufficiency, or renal failure (endstage renal disease). Initially, as renal tissue loses function, there are few abnormalities because the remaining tissue increases its performance (renal functional adaptation); a loss of 75% of renal tissue produces a fall in GFR to only

Decreased renal function interferes with the kidneys' ability to maintain fluid and electrolyte homeostasis. Changes proceed predictably, but considerable overlap and individual variation exist. The ability to concentrate urine declines early and is followed by decreases in ability to excrete phosphate, acid, and K. When renal failure is advanced (GFR ≤ 10 mL/min/1.73 m2), the ability to dilute urine is lost; thus urine osmolality is usually fixed close to that of plasma (300 to 320 mOsm/kg), and urinary volume does

Plasma concentrations of creatinine and urea (which are highly dependent on glomerular filtration) begin a nonlinear rise as GFR diminishes. These changes are minimal early on. When the GFR falls below 10 mL/min/1.73 m2 (normal = 100 mL/min/1.73 m2), their levels increase rapidly and are usually associated with systemic manifestations (uremia). Urea and creatinine are not major contributors to the uremic symptoms; they are markers for many other substances

Despite a diminishing GFR, Na and water balance is well maintained by increased fractional excretion of Na and a normal response to thirst. Thus, the plasma Na concentration is typically normal, and hypervolemia is infrequent unless dietary intake of Na or water is very restricted or excessive. Heart failure can occur from Na and water overload, particularly in patients with decreased cardiac reserve.

Chronic renal failure (CRF) is the progressive loss of kidney function. The kidneys attempt to compensate for renal damage by hyperfiltration (excessive straining of the blood) within the remaining functional nephrons (filtering units that consist of a glomerulus and corresponding tubule). Over time, hyperfiltration causes further loss of function.

Chronic loss of function causes generalized wasting (shrinking in size) and progressive scarring within all parts of the kidneys. In time, overall scarring obscures the site of the initial damage. Yet, it is not until over 70% of the normal combined function of both kidneys is lost that most patients begin to experience symptoms of kidney failure.

Types Chronic renal failure (CRF) can be classified by the site (location) of primary damage:  Pre-renal CRF  Post-renal CRF (obstructive uropathy)  Renal CRF

The cause for CRF sometimes can be determined by a detailed medical history, a comprehensive physical examination, and laboratory studies. Even a kidney biopsy may be inconclusive, because all forms of kidney failure eventually progress to diffuse scarring and look the same on kidney biopsy. The most common causes for CRF are diabetes and high blood pressure (hypertension.)

Pre-Renal CRF  Some medical conditions cause continuous hypoperfusion (low blood flow) of the kidneys, leading to kidney atrophy (shrinking), loss of nephron function, and chronic renal failure (CRF).  These conditions include poor cardiac function, chronic liver failure, and atherosclerosis ("hardening") of the renal arteries.  Each of these conditions can induce ischemic nephropathy.

Post-Renal CRF Interference with the normal flow of urine can produce backpressure within the kidneys, can damage nephrons, and lead to obstructive uropathy, a disease of the urinary tract. Bladder outlet obstruction due to an enlarged prostate gland or bladder stone  Neurogenic bladder, an overdistended bladder caused by impaired communicator nerve fibers from the bladder to the spinal cord  Kidney stones in both ureters, the tubes that pass urine from each kidney to the bladder  Obstruction of the tubules,the end channels of the renal nephrons  Retroperitoneal fibrosis, the formation of fiberlike tissue behind the peritoneum, the membrane that lines the abdominal cavity  Vesicoureteral reflux (VUR), the backward flow of urine from the bladder into a ureter

Renal CRF Chronic renal failure caused by changes within the kidneys, is called renal CRF, and is broadly categorized as follows:  Diabetic nephropathy, kidney disease associated with diabetes; the most common cause of CRF  Hypertension nephrosclerosis, a condition that occurs with increased frequency in African Americans; the second leading cause of CRF  Chronic glomerular nephritis, a condition caused by diseases that affect the glomeruli and bring about progressive dysfunction  Chronic interstitial nephritis, a condition caused by disorders that ultimately lead to progressive scarring of the interstitium  Renal vascular CRF, large vessel abnormalities such as renal artery stenosis (narrowing of the

Signs and Symptoms

Chronic renal failure (CRF) usually produces symptoms when renal function — which is measured as the glomerular filtration rate (GFR) — falls below 30 milliliters per minute (< 30 mL/min). This is approximately 30% of the normal value.

Uremic symptoms can affect every organ system, most noticeably the following:  Neurological system–cognitive impairment, personality change, asterixis (motor disturbance that affects groups of muscles), seizures (rare)  Gastrointestinal system–nausea, vomiting, food distaste (often described as bland, metallic, "like cardboard")  Blood-forming system–anemia due to erythropoetin deficiency, easy bruising and bleeding due to abnormal platelets  Pulmonary system–fluid in the lungs, with breathing difficulties  Cardiovascular system –chest pain due to inflammation of the sac surrounding the heart (pericarditis) and pericardial effusion (fluid accumulation around the heart)  Skin –generalized itching

Diagnosis  Chronic renal failure (CRF) is diagnosed by the observation of a combination of symptoms and elevated blood urea nitrogen (BUN) and creatinine (Cr) levels. The following abnormalities found in the blood may signal CRF:  Anemia (low red blood cell count)  High level of parathyroid hormone  Hypocalcemia (low blood level of calcium)  Hyperphosphatemia (high blood level of phosphate)  Hyperkalemia (high blood level of potassium)  Hyponatremia (low blood level of sodium)  Low blood level of bicarbonate

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With the loss of kidney function, phosphate accumulates in the blood. Excess phosphate in the blood reduces levels of blood calcium, and low blood calcium levels trigger the parathyroid gland (located in the neck) to release more parathyroid hormone (PTH). PTH then dissolves bone tissue to release stored calcium and raise the level of calcium in the blood. This chronic cycle of events is called secondary hyperthyroidism. The net result of this condition is the development of metabolic bone disease (renal osteodystrophy). These patients are at risk for bone fractures, bone and muscle

Acute renal failure (ARF)

is the rapid breakdown of renal (kidney) function that occurs when high levels of uremic toxins (waste products of the body's metabolism) accumulate in the blood. ARF occurs when the kidneys are unable to excrete (discharge) the daily load of toxins in the urine.

Based on the amount of urine that is excreted over a 24-hour period, patients with ARF are separated into two groups:  Oliguric: patients who excrete less than 500 milliliters per day (< 16 oz/day)  Nonoliguric: patients who excrete more than 500 milliliters per day (> 16 oz/day) In nonoliguric patients, the urine is of poor quality (i.e., contains little waste) because the blood is not well

Both kidneys are failing when ARF occurs. One normally functioning kidney can maintain adequate blood filtering.

The three types of ARF are named for their location within the renal (kidney) system:
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Prerenal ARF Postrenal ARF Intrinsic renal ARF

Prerenal Acute Renal Failure (ARF)

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Some of the most notable causes of prerenal ARF are dehydration, heart failure, sepsis (severe infection), and severe blood loss. Prerenal ARF is associated with a number of preexisting medical conditions, such as atherosclerosis ("hardening" of the arteries with fatty deposits), which reduces blood flow. Dehydration caused by drastically reduced fluid intake or excessive use of diuretics (water pills) is a major cause of prerenal ARF. Many people with severe heart conditions are kept slightly dehydrated by the diuretics they take to prevent fluid buildup in their lungs, and they often have reduced blood flow (underperfusion) to the kidneys. Risk Factors Atherosclerosis Blood loss

Postrenal Acute Renal Failure (ARF)
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Some of the most notable causes of postrenal ARF include the following: Bladder outlet obstruction due to an enlarged prostate gland or bladder stone Kidney stones in both ureters (tubes that pass urine from each kidney to the bladder) or in patients with one kidney Neurogenic bladder (overdistended bladder caused by inability of the bladder to empty) Tubule obstruction (end channels of the renal nephrons) Renal injury (usually sustained in an automobile accident or while playing a sport) Retroperitoneal fibrosis (formation of fibrous tissue behind the peritoneum—the membrane that lines the abdominal cavity)

Intrinsic Acute Renal Failure (ARF)
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The causes can be classified as follows: Vascular disease
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Glomerulonephritis (GN) and vasculitis (inflammation of blood vessels) Renal artery obstruction (atherosclerosis, thrombosis) Renal vein obstruction (thrombosis) TTP-HUS (low blood platelet and red blood cell counts)

Diseases of tubules and interstitium (space between parts of tissue)
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Amyloidosis (deposition of proteins in kidney tissues) Interstitial nephritis (associated with allergy or infection)

Acute tubular necrosis

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Intrinsic ARF accounts for approximately 40% of the cases of acute renal failure. Nearly 90% of intrinsic ARF cases are caused by ischemia or toxins, both of which lead to acute tubular necrosis (ATN). Ischemic ARF is associated with reduced blood flow to the kidneys (renal hypoperfusion), which leads to tissue death and irreversible kidney failure. Ischemic ARF occurs most frequently when there is hemorrhage (blood loss), trauma, or sepsis (severe infection), and in patients undergoing major cardiovascular surgery.

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Many types of medication can cause nephrotoxic intrinsic ARF, and the effect seems to be dose related. Most cases occur in the elderly and in patients with chronic renal failure (CRF). Toxins taken into the body that can trigger intrinsic ARF include the following: Antibiotics (e.g., acyclovir, roscarnet) Chemotherapeutic drugs (used to treat cancer, e.g., cisplatin, ifosfamide) Cyclosporine Radiocontrast dyes (used in imaging

Some toxins are released by tissues as a result of injury or are created by electrolyte imbalance. Some endogenous toxins that trigger nephrotoxic ARF include the following: Rhabdomyolysis (release of myoglobin in the urine resulting from the destruction of muscle tissue) caused by the following:
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Intoxication (e.g., alcohol, cocaine) Seizure Traumatic crush injury

Hypercalcemia (high level of calcium in the blood) caused by the following:
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Deposition of calcium in tissue Vasoconstriction (reduced diameter of blood vessels)

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Both ischemic and nephrotoxic ARF cause acute tubular necrosis (ATN), but ATN is less pronounced in nephrotoxic ARF. Allergic interstitial nephritis can be triggered by several different types of drugs. The most common are: antibiotics (e.g., penicillin, cephalosporins) and nonsteroidal anti-inflammatory drugs (e.g., acetaminophen, ibuprofen).

Signs and Symptoms  Fever, rash, arthralgia (joint pain)— associated with allergic interstitial nephritis  Flank pain—associated with renal artery or vein obstruction, severe glomerulonephritis  Headache, dizziness, confusion, seizure—associated with malignant hypertension  Oliguria (reduced urination), edema (swelling), hypertension—associated with glomerulonephritis, vasculitis  Papilledema (swollen optic disk),

Complications Because excretion of sodium and potassium is impaired, levels of these minerals and the level of chloride in the blood become elevated. This condition is known as metabolic acidosis. Several other complications may occur during the course of intrinsic ARF, including the following:  Hyperkalemia (high level of potassium in the blood)  Hypermagnamesia (high level of magnesium in the blood)  Hyperphosphatemia (high level of phosphates in the blood)  Hypocalcemia (low level of calcium in the blood)  Intravascular overload (excess fluid in the

Diagnosis  Diagnosis is based on results from blood tests and urinalysis, and on the patient's medical history and signs and symptoms.  Blood test results that show high levels of creatinine indicate renal ischemia, atheroembolism, or exposure to radiocontrast dye. Severe anemia (low red blood count) may indicate TTP-HUS. Hyperkalemia (high level of potassium), hyperphosphatemia (high level of phosphorous), and hypocalcemia (low level of calcium) occur in rhabdomyolysis.  Urinalysis shows many red and white cells in the urine, and the level of sodium may be high. Proteinuria is a common finding. Mild proteinuria suggests that failure is caused by injured tubules. Moderate

Prognosis  Before the development of renal replacement therapy (RRT), many people with ARF died from severe electrolyte imbalance (hyperkalemia, acidosis) or from the uremic toxins themselves.  Patients with ARF are at risk for numerous complications that may lead to death, such as seizures, bleeding, and coma. Since dialysis effectively treats the lifethreatening complications of ARF, advanced age and underlying diseases are more likely to determine the risk for a

Oliguric ARF patients continue to have a high mortality rate, despite the availability of RRT. Almost uniformly, these patients have other acute and/or chronic medical problems. Patients with nonoliguric ARF tend to have a more favorable prognosis and are often easier to treat. Nonoliguric ARF patients often have fewer systemwide complications because their condition typically is caused by

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