Urinary SystemRelated diseases and Peritoneal Dialysis A presentation by Rowell Angeles
Acute Glomerulonephritis(AGN) Acute glomerulonephritis (AGN) is active inflammation in the glomeruli. Each kidney is composed of about 1 million microscopic filtering "screens" known as glomeruli that selectively remove uremic waste products. The inflammatory process usually begins with an infection or injury (e.g., burn, trauma), then the protective immune system fights off the infection, scar tissue forms, and the process is complete. There are many diseases that cause an active inflammation within the glomeruli. Some of these diseases are systemic (i.e., other parts of the body are involved at the same time) and some occur solely in the glomeruli. When there is active inflammation within the kidney, scar tissue may replace normal, functional kidney tissue and cause irreversible renal impairment. The severity and extent of glomerular damage—focal (confined) or diffuse (widespread)—determines how the disease is manifested. Glomerular damage can appear as subacute renal failure, progressive chronic renal failure (CRF); or simply a urinary abnormality such as hematuria (blood in the urine) or proteinuria (excess protein in the urine).
Causes In diffuse glomerulonephritis (GN), all of the glomeruli are aggressively attacked, leading to acute renal failure (ARF). Disorders that attack several organs and cause diffuse GN are referred to as secondary causes. Secondary causes of diffuse GN include the following: Cryoglobulinemia Goodpasteur’s syndrome (membranous antiglomerular basement membrane disease) Lupus nephritis Schönlein-Henochpurpura Vasculitis (e.g., Wegener's granulomatosis, periarteritisnodosa) Primary diseases that solely affect the kidneys and cause AGN, include the following: Immunoglobulin A nephropathy (IgA nephropathy, Berger’s disease) Membranoproliferative nephritis (type of kidney inflammation) Postinfectious GN (GN that results after an infection)
Signs & Symptoms Patients who have secondary causes of AGN often exhibit these symptoms: Cough with blood-tinged sputum Fever Joint or muscle pain Rash
Diagnosis & Treatment Diagnosis Patients with acute glomerulonephritis (AGN) have an active urinary sediment. This means that signs of active kidney inflammation can be detected when the urine is examined under the microscope. Such signs include red blood cells, white blood cells, proteinuria (blood proteins in the urine), and "casts" of cells that have leaked through the glomeruli and have reached the tubule, where they develop into cylindrical forms. A kidney biopsy is essential to establish a diagnosis of AGN, determine the cause, and create an effective treatment plan. Treatment The goal of treatment is to stop the ongoing inflammation and lessen the degree of scarring that ensues. Depending on the diagnosis, there are different treatment strategies. Often the treatment warrants a regimen of immunosuppressive drugs to limit the immune system’s activity. This decreases the degree of inflammation and subsequent irreversible scarring.
Acute renal failure (ARF) Acute renal failure (ARF) or acute kidney injury (AKI), as it is now referred to in the literature, is defined as an abrupt or rapid decline in renal filtration function. This condition is usually marked by a rise in serum creatinine concentration or azotemia (a rise in blood urea nitrogen [BUN] concentration). However, immediately after a kidney injury, BUN or creatinine levels may be normal, and the only sign of a kidney injury may be decreased urine production. A rise in the creatinine level can result from medications (eg, cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion. A rise in the BUN level can occur without renal injury, resulting instead from such sources as GI or mucosal bleeding, steroid use, or protein loading, so a careful inventory must be taken before determining if a kidney injury is present.
Acute renal failure (ARF) AKI may be classified into 3 general categories, as follows: Prerenal—as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons Intrinsic—in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage Postrenal—from obstruction to the passage of urine. While this classification is useful in establishing a differential diagnosis, many pathophysiologic features are shared among the different categories. Patients who develop AKI can be oliguric or nonoliguric, have a rapid or slow rise in creatinine levels, and may have qualitative differences in urine solute concentrations and cellular content. This lack of a uniform clinical presentation reflects the variable nature of the injury. Classifying AKI as oliguric or nonoliguric based on daily urine excretion has prognostic value. Oliguria is defined as a daily urine volume of less than 400 mL/d and has a worse prognosis, except in prerenal failure. Anuria is defined as a urine output of less than 100 mL/d and, if abrupt in onset, suggests bilateral obstruction or catastrophic injury to both kidneys. Stratification of renal failure along these lines helps in decision-making (eg, timing of dialysis) and can be an important criterion for patient response to therapy.
Causes The myriad causes of acute kidney injury are commonly categorised into prerenal, intrinsic, and postrenal. Prerenal Prerenal causes of AKI are those that decrease effective blood flow to the kidney. These include low blood volume, low blood pressure, and heart failure. Changes to the blood vessels supplying the kidney can also lead to prerenal AKI. These include renal artery stenosis, which is a narrowing of the renal artery that supplies the kidney, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney. Intrinsic Those causes that lead to damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. Postrenal Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, or an obstructed urinary catheter.
Diagnosis Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria. Specific criteria exist for the diagnosis of AKI: Rapid time course (less than 48 hours) Reduction of kidney function Rise in serum creatinine Absolute increase in serum creatinine of ≥0.3 mg/dl (≥26.4 μmol/l) Percentage increase in serum creatinine of ≥50% Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours RIFLE criteria Another commonly used set of consensus criteria, called the RIFLE criteria, aid in the diagnosis and risk stratification of patients with AKI: Risk: serum creatinine increased 1.5 times or urine production of <0.5 ml/kg for 6 hours Injury: doubling of creatinine or urine production <0.5 ml/kg for 12 hours Failure: tripling of creatinine or creatinine >355 μmol/l (with a rise of >44) OR urine output below 0.3 ml/kg for 24 hours Loss: persistent AKI or complete loss of kidney function for more than 4 weeks End-stage renal disease: complete loss of kidney function for more than 3 months
Treatment The management of AKI hinges on identification and treatment of the underlying cause. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, and others. Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.
Acute tubular necrosis (ATN) Acute tubular necrosis or (ATN) is a medical condition involving the death of tubular cells that form the tubule that transports urine to the ureters while reabsorbing 99% of the water (and highly concentrating the salts and metabolic byproducts). Tubular cells continually replace themselves and if the cause of ATN is removed then recovery is likely. ATN presents with acute renal failure (ARF) and is one of the most common causes of ARF. The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.
Causes Acute tubular necrosis (ATN) is caused by lack of oxygen to the kidney tissues (ischemia of the kidneys), or by exposure to materials that are poisonous to the kidney (nephrotoxic agents). The internal structures of the kidney, particularly the tissues of the kidney tubule, become damaged or destroyed. ATN is one of the most common structural changes that can lead to acute renal failure. ATN is one of the most common causes of kidney failure in hospitalized patients. Risks for acute tubular necrosis include: Blood transfusion reaction Injury or trauma that damages the muscles Recent major surgery Septic shock or other forms of shock Severe low blood pressure (hypotension) that lasts longer than 30 minutes Any condition that reduces the amount of blood being pumped by the heart can cause ATN. Liver disease and damage caused by diabetes (diabetic nephropathy) may make a person more susceptible to the condition. ATN can be caused by: Exposure to substances that are toxic to the kidneys (such as aminoglycoside antibiotics) Antifungal agents (such as amphotericin) Dye used for x-ray (radiographic) studies
Symptoms Symptoms Decreased consciousness Coma Delirium or confusion Drowsy, lethargic, hard to arouse Decreased urine output or no urine output General swelling, fluid retention Nausea, vomiting Note: Other symptoms of acute kidney failure may also be present.
Diagnosis Exams and Tests Examination usually indicates acute kidney failure. There may be signs of fluid overload, including abnormal sounds on listening to the heart and lungs with a stethoscope (auscultation). Other signs include: BUN and serum creatinine levels may increase Fractional excretion of sodium and of urea may be relatively high Kidney biopsy may show acute tubular necrosis (but a biopsy is rarely done) Urinalysis may show casts, kidney tubular cells, and red blood cells Urine sodium may be high Urine specific gravity and osmolarity urine indicate dilute urine
Treatment In most people, acute tubular necrosis is reversible. The goal of treatment is to prevent life-threatening complications of acute kidney failure during the time the lesion is present. Treatment focuses on preventing the excess build-up of fluids and wastes, while allowing the kidneys to heal. Patents should be watched for deterioration of kidney function. Treatment can include: Identifying and treating the underlying cause of the problem Restricting fluid intake to a volume equal to the volume of urine produced Restricting substances normally removed by the kidneys (such as protein, sodium, potassium) to minimize their buildup in the body Taking medications to help control potassium levels in the bloodstream Taking water pills (diuretics) to increase fluid removal from the kidney
Treatment Dialysis can remove excess waste and fluids. This can make you feel better, and may make the kidney failure easier to control. Dialysis may not be necessary for all people, but is often lifesaving, especially if serum potassium is dangerously high. Dialysis may be needed in the following cases: Decreased mental status Fluid overload Increased potassium levels Pericarditis Total lack of urine production Uncontrolled buildup of nitrogen waste products
Urinary tract Infection (UTI) Urinary tract infections are a serious health problem affecting millions of people each year. Infections of the urinary tract are the second most common type of infection in the body. Urinary tract infections (UTIs) account for about 8.3 million doctor visits each year. Women are especially prone to UTIs for reasons that are not yet well understood. One woman in five develops a UTI during her lifetime. UTIs in men are not as common as in women but can be very serious when they do occur. The urinary system consists of the kidneys, ureters, bladder, and urethra. The key elements in the system are the kidneys, a pair of purplish-brown organs located below the ribs toward the middle of the back. The kidneys remove excess liquid and wastes from the blood in the form of urine, keep a stable balance of salts and other substances in the blood, and produce a hormone that aids the formation of red blood cells. Narrow tubes called ureters carry urine from the kidneys to the bladder, a sack-like organ in the lower abdomen. Urine is stored in the bladder and emptied through the urethra. The average adult passes about a quart and a half of urine each day. The amount of urine varies, depending on the fluids and foods a person consumes. The volume formed at night is about half that formed in the daytime.
Causes Normally, urine is sterile. It is usually free of bacteria, viruses, and fungi but does contain fluids, salts, and waste products. An infection occurs when tiny organisms, usually bacteria from the digestive tract, cling to the opening of the urethra and begin to multiply. The urethra is the tube that carries urine from the bladder to outside the body. Most infections arise from one type of bacteria, Escherichia coli (E. coli), which normally lives in the colon. In many cases, bacteria first travel to the urethra. When bacteria multiply, an infection can occur. An infection limited to the urethra is called urethritis. If bacteria move to the bladder and multiply, a bladder infection, called cystitis, results. If the infection is not treated promptly, bacteria may then travel further up the ureters to multiply and infect the kidneys. A kidney infection is called pyelonephritis. Microorganisms called Chlamydia and Mycoplasma may also cause UTIs in both men and women, but these infections tend to remain limited to the urethra and reproductive system. Unlike E. coli, Chlamydia and Mycoplasma may be sexually transmitted, and infections require treatment of both partners. The urinary system is structured in a way that helps ward off infection. The ureters and bladder normally prevent urine from backing up toward the kidneys, and the flow of urine from the bladder helps wash bacteria out of the body. In men, the prostate gland produces secretions that slow bacterial growth. In both sexes, immune defenses also prevent infection. But despite these safeguards, infections still occur.
Symptoms Not everyone with a UTI has symptoms, but most people get at least some symptoms. These may include a frequent urge to urinate and a painful, burning feeling in the area of the bladder or urethra during urination. It is not unusual to feel bad all over -- tired, shaky, washed out -- and to feel pain even when not urinating. Often women feel an uncomfortable pressure above the pubic bone, and some men experience a fullness in the rectum. It is common for a person with a urinary infection to complain that, despite the urge to urinate, only a small amount of urine is passed. The urine itself may look milky or cloudy, even reddish if blood is present. Normally, a UTI does not cause fever if it is in the bladder or urethra. A fever may mean that the infection has reached the kidneys. Other symptoms of a kidney infection include pain in the back or side below the ribs, nausea, or vomiting. In children, symptoms of a urinary infection may be overlooked or attributed to another disorder. A UTI should be considered when a child or infant seems irritable, is not eating normally, has an unexplained fever that does not go away, has incontinence or loose bowels, or is not thriving. Unlike adults, children are more likely to have fever and no other symptoms. This can happen to both boys and girls. The child should be seen by a doctor if there are any questions about these symptoms, especially a change in the child's urinary pattern.
Treatment UTIs are treated with antibacterial drugs. The choice of drug and length of treatment depend on the patient's history and the urine tests that identify the offending bacteria. The sensitivity test is especially useful in helping the doctor select the most effective drug. The drugs most often used to treat routine, uncomplicated UTIs are trimethoprim (Trimpex), trimethoprim/sulfamethoxazole (Bactrim, Septra, Cotrim), amoxicillin (Amoxil, Trimox, Wymox), nitrofurantoin (Macrodantin, Furadantin), and ampicillin (Omnipen, Polycillin, Principen, Totacillin). A class of drugs called quinolones includes four drugs approved in recent years for treating UTI. These drugs include ofloxacin (Floxin), norfloxacin (Noroxin), ciprofloxacin (Cipro), and trovafloxin (Trovan). Often, a UTI can be cured with 1 or 2 days of treatment if the infection is not complicated by an obstruction or other disorder. Still, many doctors ask their patients to take antibiotics for a week or two to ensure that the infection has been cured. Single-dose treatment is not recommended for some groups of patients, for example, those who have delayed treatment or have signs of a kidney infection, patients with diabetes or structural abnormalities, or men who have prostate infections. Longer treatment is also needed by patients with infections caused by Mycoplasma or Chlamydia, which are usually treated with tetracycline, trimethoprim/sulfamethoxazole (TMP/SMZ), or doxycycline. A followup urinalysis helps to confirm that the urinary tract is infection-free. It is important to take the full course of treatment because symptoms may disappear before the infection is fully cleared.
Continuous Ambulatory Peritoneal Dialysis (CAPD) Dialysis is a process by which waste products are removed from the blood and excess fluid is removed from the body. There are two types of dialysis: peritoneal dialysis or continuous ambulatory peritoneal dialysis (CAPD) and hemodialysis.
Continuous Ambulatory Peritoneal Dialysis (CAPD) How CAPD Works Continuous ambulatory peritoneal dialysis (CAPD) involves instilling 2 to 3 liters (quarts) of fluid at a time into the person's abdominal (or "peritoneal") cavity through a flexible plastic catheter that is implanted in the abdominal wall. The fluid is allowed to remain in the abdominal cavity for a period of hours, gradually absorbing waste products and toxins from the body; it is then drained out and replaced with fresh fluid. This procedure of fluid exchange is performed by the patient, and is done 4-5 times a day, 7 days a week. The procedure involves careful use of sterile technique and constant monitoring of blood pressure, fluid volumes, and weights, so many patients are not able to perform this type of dialysis. A variation on this procedure is dialysis with a cycler, in which the patient performs one or two fluid exchanges daily, as described above, and then hooks up to an automatic cycler, which performs several more exchanges during the night as the patient sleeps.
Continuous Ambulatory Peritoneal Dialysis (CAPD) Preparing for CAPD Like hemodialysis, CAPD requires preparatory surgery. A flexible catheter must be surgically implanted in the abdominal wall and then requires several weeks to scar firmly in place. Advantages of CAPD Flexibility in Schedule - Although CAPD requires a great deal of work on the part of the patient, patients who have the manual dexterity and ability to learn the procedure and the ability to be compulsive about record keeping and sterile technique find that this type of dialysis gives them more flexibility of schedule and greater freedom to work, go to school, and be active in general. Flexibility in Diet - CAPD also allows a more liberal diet than hemodialysis, because fluid and potentially harmful substances (such as potassium, salt, and protein) are continuously removed by dialysis as they are eaten, and thus do not accumulate in harmful or dangerous amounts.
Continuous Ambulatory Peritoneal Dialysis (CAPD) The main complication of this type of dialysis is infection, of which there is a risk every time an exchange is performed and every time the abdominal catheter is uncapped in order to add fluid to the abdominal cavity or to drain fluid from it. The symptoms of abdominal cavity infection, or “peritonitis,” are abdominal pain, fever, and cloudy fluid draining from the abdomen. This type of infection, which can be quite serious, is treated with antibiotics given either IV or in the dialysis fluid that is instilled into the abdomen. In order to avoid peritonitis, it is extremely important for the patient to carefully follow sterile technique every time they do a fluid exchange, which requires wearing sterile gloves and a mask, as well as using sterile disposable equipment, tubing, and dialysis fluid. Repeated episodes of peritonitis can cause scarring in the abdominal cavity, sometimes so severe that peritoneal dialysis will no longer work.