Classification Of Acute Renal Failure (Based On The Causes)

Classification Of Acute Renal Failure (Based On The Causes)

The causes of acute renal failure (ARF) are conventionally and conveniently divided into 3 categories : prerenal, renal, and postrenal.

• Prerenal ARF involves an essentially normal kidney that is responding to hypoperfusion by decreasing the glomerular filtration rate (GFR).

• Renal or intrinsic ARF refers to a condition in which the pathology lies within the kidney itself.

• Postrenal ARF is caused by an obstruction of the urinary tract. Acute tubular necrosis (ATN) is the most common cause of ARF in the renal category.

Prerenal ARF

Prerenal ARF represents the most common form of kidney injury and often leads to intrinsic ARF if it is not promptly corrected.

• Volume loss from GI, renal, cutaneous (eg, burns), and internal or external hemorrhage can result in this syndrome.

• Prerenal ARF can also result from decreased renal perfusion in patients with heart failure or shock (eg, sepsis, anaphylaxis).

• Special classes of medications that can induce prerenal ARF in volume-depleted states are angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), which are otherwise safely tolerated and beneficial in most patients with chronic kidney disease.

• Arteriolar vasoconstriction leading to prerenal ARF can occur in hypercalcemic states, with the use of radiocontrast agents, nonsteroidal anti-inflammatory drugs (NSAIDs), amphotereicin, calcineurin inhibitors, norepinephrine, and other pressor agents.

• The hepatorenal syndrome can also be considered a form of prerenal ARF because functional renal failure develops from diffuse vasoconstriction in vessels supplying the kidney.

Renal or Intrinsic ARF

Structural injury in the kidney is the hallmark of Renal or Intrinsic ARF, and the most common form is acute tubular injury (ATN), either Ischemic or Cytotoxic. Frank necrosis is not prominent in most human cases of ATN and tends to be patchy.

• Intrarenal Vasoconstriction is the dominant mechanism for the reduced glomerular filtration rate (GFR) in patients with ATN. The mediators of this vasoconstriction are unknown, but tubular injury seems to be an important concomitant finding.
  

• Urine backflow and intratubular obstruction (from sloughed cells and debris) are causes of reduced net ultrafiltration. The importance of this mechanism is highlighted by the improvement in renal function that follows relief of such intratubular obstruction.
  

• Apart from the increase in basal renal vascular tone, the stressed renal microvasculature is more sensitive to potentially vasoconstrictive drugs and otherwise-tolerated changes in systemic blood pressure. The vasculature of the injured kidney has an impaired vasodilatory response and loses its autoregulatory behavior.

• A physiologic hallmark of ATN is a failure to maximally dilute or concentrate urine (isosthenuria). This defect is not responsive to pharmacologic doses of vasopressin. The injured kidney fails to generate and maintain a high medullary solute gradient because the accumulation of solute in the medulla depends on normal distal nephron function.
  

• Failure to excrete concentrated urine, even in the presence of oliguria, is a helpful diagnostic clue to distinguish prerenal from intrinsic renal disease, in which urine osmolality is less than 300 mOsm/kg. In prerenal azotemia, urine osmolality is typically more than 500 mOsm/kg.

• Glomerulonephritis can be a cause of ARF and usually falls into a class referred to as rapidly progressive glomerulonephritis (RPGN). The pathologic correlation of RPGN is the presence of glomerular crescents (glomerular injury) on biopsy; if more than 50% of glomeruli contain crescents, this usually results in a significant decline in renal function. Although comparatively rare, acute glomerulonephritides should be part of the diagnostic consideration in cases of ARF.

Postrenal ARF

Mechanical obstruction of the urinary collecting system, including the renal pelvis, ureters, bladder, or urethra, results in obstructive uropathy or postrenal ARF.

• If the site of obstruction is unilateral, then a rise in the serum creatinine level may not be apparent due to contralateral renal function. Although the serum creatinine level may remain low with unilateral obstruction, a significant loss of GFR occurs, and patients with partial obstruction may develop progressive loss of GFR if the obstruction is not relieved. Causes of obstruction include stone disease; stricture; and intraluminal, extraluminal, or intramural tumors.

• Bilateral obstruction is usually a result of prostate enlargement or tumors in men and urologic or gynecologic tumors in women.

• Patients who develop anuria typically have obstruction at the level of the bladder or downstream to it.

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Acute Renal Failure (ARF) - Chronic Renal Insufficiency (CRI) - End Stage Renal Disease (ESRD)

Acute Renal Failure (ARF) VS Chronic Renal Insufficiency (CRI)
VS
End Stage Renal Disease (ESRD)

Acute Renal Failure (ARF)

This is kidney failure that happens rather suddenly, where something has caused the kidneys to shutdown. This may be due to infection, drugs (prescription, over-the-counter, recreational), traumatic injury, major surgery, nephrotoxic poisons, etc.

Emergency dialysis may be needed until the situation resolves and the kidneys begin functioning again (this might take a short time, or months, or it might be permanent). While more acute episodes are possible in the case of IgAN (we often refer to them as "flare-ups"), IgA nephropathy is a condition that mainly causes chronic renal insufficiency (CRI), not usually acute renal failure (ARF).

However, some people may experience spontaneously-reversing acute renal failure as well. The latter are cases where serum creatinine goes up dramatically but later returns to a more normal baseline. In such cases, dialysis may be needed until the condition improves. ARF in the context of IgAN is usually more associated with the person developing a flare-up of HSP.

Chronic Renal Insufficiency (CRI)

This is when a disease such as IgA nephropathy slowly and gradually destroys the filtering capacity of the kidneys. It is sometimes referred to as Progressive Renal Insufficiency, Chronic Kidney Disease or Chronic Renal Failure (CRF). This kind of damage cannot currently be repaired, and as such, it is Irreversible. A person may have chronic renal failure for many years, even decades, before dialysis or a kidney transplant become necessary.

Chronic renal insufficiency does not, by itself, mean complete shutdown of the kidneys, and a person with chronic renal insufficiency may still pass urine normally, and may have more than enough kidney function left for normal functioning of the body. Note that you cannot judge the efficiency of your kidneys by the amount of urine you produce. People with quite advanced renal insufficiency, and even people on dialysis may still produce a fair amount of urine. But this does not mean that the kidneys are filtering waste nor regulating serum electrolyte levels efficiently.

Chronic renal insufficiency itself causes more loss of kidney function. One important aspect of kidney disease is that, once a kidney is damaged by it to a certain degree, it continues to deteriorate even if the underlying kidney disease can or could be cured. This is commonly referred to as the Point of No Return (PNR).

Classification Of Chronic Renal Insufficiency

Early Chronic Renal Insufficiency (Stages 1 to 2)
Advanced Chronic Renal Insufficiency (Stages 3 to 4)

Late Chronic Renal Insufficiency (Stages 5) - ESRD

What happens is that the chronic renal insufficiency (CRI) continues to progress on its own, scarring of the glomeruli continues, and kidney function continues to gradually decline. It's possible that controlling blood pressure with an ACE inhibitor like Ramipril, or an Angiotensin II Receptor Blocker like Cozaar or Avapro may slow this progression of chronic renal insufficiency.

There is also beginning to be some evidence that the class of anti-cholesterol drugs called "Statins" (like Lipitor, for example) may help slow progression of CRI.

The point of no return is generally considered to be when serum creatinine reaches 2.0 mg/dl in U.S. measurements, or about 175 umol/L in international SI measurement.

End-Stage Renal Disease (ESRD)

As Chronic Renal Insufficiency continues and progresses, the person may eventually reach the point where it is considered to be End-Stage Renal Disease (ESRD) also known as Late Chronic Renal Insufficiency. It is at this stage that you are on the threshold of needing renal replacement therapy (any form of dialysis, or a kidney transplant).

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Chronic Kidney Disease Staging

CHRONIC KIDNEY DISEASE STAGING

Introduction

Chronic kidney disease occur whenever the glomerular filtration rate (GFR) is less than 60 mL/min/1.73 m2 for about 3 months, with or without kidney damage, for examples : pathologic abnormalities or markers of damage including (proteinuria or kidney stones).

Classification - Staging

There are five stages of chronic kidney disease based on the GFR (Cockcroft-Gault Formula) :

* Stage 1: Normal or increased GFR (>= 90 mL/min/1.73m2) with evidence of kidney damage.

The emphasis is on diagnosis, treatment and prevention of disease progression.

* Stage 2: Mildly decreased GFR (60-89 mL/min/1.73m2) with evidence of kidney damage.

There is still interest in diagnosis and treatment of the underlying cause but the emphasis is shifting towards prevention of disease progression.

* Stage 3: Moderately decreased GFR (30-59 mL/min/1.73m2).

The emphasis is still on preventing disease progression but the evaluation and treatment of complications are becoming more of an issue.

* Stage 4: Severely decreased GFR (15-29 mL/min/1.73m2).

The emphasis is generally on treating complications and preparing for dialysis or kidney transplantation.

* Stage 5: Very little GFR left (<15 ml/min/1.73m2).

Treating complications becomes increasingly difficult and dialysis is usually started at this point.

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The Cockcroft-Gault Formula - Creatinine Clearance Estimation (By Using GFR)

The Cockcroft-Gault Formula - Creatinine Clearance Estimation
(By Using GFR)

INTRODUCTION

The formula gives the Glomerular Filtration Rate, in ml/hour. In other words, it estimates the rate at which plasma ultrafiltrate is produced by the kidneys.

This is a quick and dirty estimate, and gives a good estimate only when creatinine clearance is stable. If the creatinine concentration is rising, applying this formula would be highly inaccurate.

For most purposes, however, the Cockcroft-Gault formula is the most common formula used by physicians to estimate creatinine clearance, and thus Glomerular Filtration Rate (ml/min/1.73 m2).

THE FORMULA

The Cockcroft-Gault Formula is Used to calculate Creatinine Clearance.

MEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine(mg/dl)) X 1

WOMEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine(mg/dl)) X 0.85

OR

MEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine/88.6(mcmol/L)) X 1

WOMEN : GFR = (140 - age) x Weight (kg) / (72 x serum creatinine/88.6(mcmol/L)) X 0.85

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Creatinine and Creatinine Clearance

Creatinine and Creatinine Clearance

Creatinine and creatinine clearance tests measure the level of the waste product creatinine in your blood and urine. These tests tell how well your kidneys are working. The substance creatine is formed when food is changed into energy through a process called metabolism. Creatine is broken down into another substance called creatinine, which is taken out of your blood by the kidneys and then passed out of your body in urine.

Creatinine is made at a steady rate and is not affected by diet or by normal physical activities. If your kidneys are damaged and cannot work normally, the amount of creatinine in your urine goes down while its level in your blood goes up.

Three types of tests on creatinine can be done:

Blood Creatinine Level

The blood creatinine level shows how well your kidneys are working. A high creatinine level may mean your kidneys are not working properly. The amount of creatinine in the blood depends partly on the amount of muscle tissue you have; men generally have higher creatinine levels than women.

Creatinine Clearance Test

A creatinine clearance test measures how well creatinine is removed from your blood by your kidneys. A creatinine clearance test gives better information than a blood creatinine test on how well your kidneys are working. A creatinine clearance test is done on both a blood sample and on a sample of urine collected over 24 hours (24-hour urine sample).

Blood Urea Nitrogen-to-Creatinine ratio (BUN:creatinine)

The levels of blood creatinine and blood urea nitrogen (BUN) can be used to find the BUN-to-creatinine ratio. A BUN-to-creatinine ratio can help your doctor check for problems, such as dehydration, that may cause abnormal BUN and creatinine levels.

Urea is a waste product made when protein is broken down in your body. Urea is made in the liver and passed out of your body in the urine. A blood urea nitrogen (BUN) test measures the amount of urea in your blood. Like creatinine, it can help your doctor see how well your kidneys are working.

Why It Is Done?

A blood creatinine level or a creatinine clearance test is done to:

* See if your kidneys are working normally.
* See if your kidney disease is changing.
* See how well the kidneys work in people who take medicines that can cause kidney damage.
* See if severe dehydration is present. Dehydration generally causes BUN levels to rise more than creatinine levels. This causes a high BUN-to-creatinine ratio. Kidney disease or blockage of the flow of urine from your kidney causes both BUN and creatinine levels to rise.

How To Prepare?

Do not do any strenuous exercise for 2 days (48 hours) before having creatinine tests.

Do not eat more than 8oz of meat, especially beef, or other protein for 24 hours before the blood creatinine test and during the creatinine clearance urine test.

It is important to drink enough fluids during the 24-hour urine collection but do not drink coffee and tea. These are diuretics that cause your body to pass more urine.

Collection of The Blood Sample & The 24-Hour Urine Sample

* Blood Sample will be taken by the Medical Proffesional - then will be examined in the Laboratory for the Blood Creatinin Level.
* After that, you can start collecting your urine in the next morning. When you first get up, empty your bladder but do not save this urine. Write down the time that you urinated to mark the beginning of your 24-hour collection period.
* For the next 24 hours, collect all your urine. Your doctor or lab will usually provide you with a large container that holds about 1 gal (4 L). The container has a small amount of preservative in it. Urinate into a small, clean container and then pour the urine into the large container. Do not touch the inside of the container with your fingers.
* Keep the large container in the refrigerator for the 24 hours.
* Empty your bladder for the final time at or just before the end of the 24-hour period. Add this urine to the large container and record the time.
* Do not get toilet paper, pubic hair, stool (feces), menstrual blood, or other foreign matter in the urine sample.

Results

Creatinine and Creatinine Clearance Tests measure Creatinine Levels in your Blood and Urine to give information about how well your kidneys are working. The creatinine clearance value is found from the amounts of creatinine in the urine and blood and from the amount of urine you pass in 24 hours. This value is the amount of blood cleared of creatinine per minute, based on your body size. Below are the normal range of the Blood Creatinine, Creatinine Clearance & BUN To Creatinin Ratio :

Blood Creatinine:

Men : 0.6–1.2 milligrams per deciliter (mg/dL) or 53-106 micromoles/L (mcmol/L)
Women : 0.5–1.1 mg/dL or 44–97 mcmol/L
Teen 0.5–1.0 mg/dL
Child 0.3–0.7 mg/dL
Newborn 0.3–1.2mg/dL

Creatinine Clearance:

Men 90–140 milliliters per minute (mL/min) or 1.78–2.32 milliters per second (mL/sec)
Women 87–107 mL/min or 1.45-1.78 mL/sec
Creatinine clearance values normally go up as you get older (normal values go down by 6.5 mL/min for every 10 years past the age of 20).

BUN-To-Creatinine Ratio

Over 12 months of age: 10:1–20:1

Infants less than 12 months of age: Up to 30:1

INTERPRETATION

High values

* High creatinine blood levels. High creatinine blood levels can mean serious kidney damage or disease is present. Kidney damage can be caused by a life-threatening infection, shock, cancer, or low blood flow to the kidneys. Other conditions that can cause high blood creatinine levels include blockage of the urinary tract (such as by a kidney stone), heart failure, dehydration, excessive blood loss that causes shock, gout, or muscle conditions (such as rhabdomyolysis, gigantism, acromegaly, myasthenia gravis, muscular dystrophy, and polymyositis). Usually a high blood creatinine level means that the creatinine clearance value is lower than normal.
* High creatinine clearance. High creatinine clearance values can be caused by strenuous exercise, muscle injury (especially crushing injuries), burns, carbon monoxide poisoning, hypothyroidism, and pregnancy.
* High BUN-to-creatinine ratio. High BUN-to-creatinine ratios occur with sudden (acute) kidney failure, which may be caused by shock or severe dehydration. A blockage in the urinary tract (such as a kidney stone) can cause a high BUN-to-creatinine ratio. A very high BUN-to-creatinine ratio may be caused by bleeding in the digestive tract or respiratory tract.

Low Values

* Low blood creatinine levels. Low blood creatinine levels can mean lower muscle mass caused by a disease, such as muscular dystrophy, or by aging. Low levels can also mean some types of severe liver disease or a diet very low in protein. Pregnancy can also cause low blood creatinine levels.
* Low creatinine clearance. Low creatinine clearance levels can mean serious kidney damage is present. Kidney damage can be from conditions such as a life-threatening infection, shock, cancer, low blood flow to the kidneys, or urinary tract blockage. Other conditions, such as heart failure, dehydration, and liver disease (cirrhosis), can also cause low creatinine clearance levels.
* Low BUN-to-creatinine ratio A low BUN-to-creatinine ratio may be associated with a diet low in protein, a severe muscle injury called rhabdomyolysis, pregnancy, cirrhosis, or syndrome of inappropriate antidiuretic hormone secretion (SIADH). SIADH sometimes occurs with lung disease, cancer, diseases of the central nervous system, and the use of certain medications.

What Affects the Test

Reasons you may not be able to have the test or why the results may not be helpful include:

* Taking medicines, such as methyldopa (Aldomet), trimethoprim (Proloprim, Trimpex), vitamin C (ascorbic acid), cimetidine (Tagamet), some diuretics, and cephalosporin antibiotics, especially cefoxitin (Mefoxin). These affect the blood creatinine levels.
* Taking medicines, such as vitamin C (ascorbic acid), phenytoin (Dilantin), some cephalosporin antibiotics, captopril, aminoglycosides (Garamycin), trimethoprim (Proloprim, Trimpex), cimetidine (Tagamet), quinine, quinidine (Cardioquin, Quinaglute, Quinidex), procainamide, and the antifungal medication amphotericin B. These affect the creatinine clearance levels.
* Taking medicines, such as cimetidine (Tagamet), steroids, and tetracycline antibiotics. These can affect the BUN-to-creatinine ratio.
* Doing strenuous exercise 2 days before creatinine clearance test.
* Eating more than 8oz of meat, especially beef, in the 24 hours before a blood creatinine test and during a creatinine clearance urine test.

What To Think About

* A high blood creatinine level is generally seen with a low creatinine clearance level because creatinine in the blood is removed by the kidneys. If the kidneys are not able to remove creatinine (low creatinine clearance), levels of creatinine in the blood go up (high blood creatinine level).
* If you are pregnant, your doctor can check the amount of creatinine in amniotic fluid to see how developed, or mature, your baby's kidneys are. This can be helpful if there is a chance your baby will be delivered early. A baby who has mature kidneys will make more creatinine than a baby whose kidneys are still developing.
* A normal blood creatinine level does not rule out kidney disease. To help see whether kidney damage may be present, a BUN level is also measured. Other tests may also be done to check for kidney disease. For more information, see the medical test Blood Urea Nitrogen.
* Creatinine levels increase more slowly than blood urea nitrogen (BUN) levels, so an increase in creatinine may mean chronic kidney problems.
* A glomerular filtration rate may be done for people with chronic kidney disease to regularly check how well the kidneys are working.
* Diabetes experts recommend that blood creatinine levels be done every year for people with diabetes. The creatinine level is used to find the glomerular filtration rate, which shows how well the kidneys are working.
* The amount of creatinine in the blood depends partly on the amount of muscle tissue; blood creatinine levels are generally higher in men than in women. Also, people who have large muscles, such as athletes, normally have above-average blood creatinine levels.
* A one-time urine sample to measure urine creatinine and sodium is sometimes done along with blood creatinine and sodium levels to help find the fractional excretion of sodium (FENA). This test can help your doctor see whether a problem with blood flow to the kidneys is caused by dehydration or shock or by damage to the kidneys themselves.

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Diuretic Induced Hypokalemia

DIURETIC INDUCED HYPOKALEMIA

INTRODUCTION

Hypokalemia is a relatively common problem with diuretic therapy. Profound hypokalemia (serum potassium concentrations ≤2.5 to 3.0 meq/L), however, is relatively rare, described in fewer than 10 to 15 percent of patients receiving high doses of diuretics, and generally only in those not receiving potassium supplementation.

The decrease in plasma concentration following prolonged administration of 50 mg of hydrochlorothiazide per day is approximately 0.5 meq/L, whereas the same dose of long-acting chlorthalidone causes a greater fall in serum potassium concentration (0.8 meq/L) [1] . In contrast, short-term administration (three days) of 50 mg of chlorthalidone and 40 mg of furosemide results in a fall in serum potassium concentration of only 0.4 and 0.2 meq/L, respectively.

The incidence and severity of hypokalemia are dose-dependent, occurring much less frequently with lower doses [5,6] . Thus, lower doses of thiazides (eg, 12.5 mg/day of hydrochlorothiazide or chlorthalidone) or loop diuretics are now widely used in the treatment of hypertension because they are as effective in blood pressure reduction with a lesser effect on electrolyte balance.

MECHANISMS

Two factors appear to be responsible for the urinary potassium wasting :

• Increased delivery of sodium and water to the aldosterone-sensitive potassium secretory site in the collecting tubules; and

• Increased secretion of aldosterone due to diuretic-induced volume depletion or due to an underlying disease such as heart failure (show figure 3) [7] .

TIME COURSE

In stable patients on a fixed diuretic dose, potassium loss, like other diuretic-induced fluid and electrolyte complications, occurs only during the first two weeks of therapy before a new steady state is established. Thus, a stable patient with a normal serum potassium concentration at three weeks is not at risk of late hypokalemia unless the diuretic dose is increased, extrarenal potassium losses increase, or dietary potassium intake is reduced.

CLINICAL SIGNIFICANCE

The development of hypokalemia is of greatest concern in patients with underlying heart disease, cirrhosis, or hypertension:

* Potassium depletion can lead to cardiac arrhythmias, particularly in the presence of concurrent digitalis therapy or a serum potassium concentration ≤3.0 meq/L [1] . In addition, hypokalemia may contribute to an increased incidence of sudden death in patients with hypertension and left ventricular hypertrophy.

* Hypokalemia (serum potassium less than 3.5 meq/L) can precipitate hepatic coma in some patients with advanced cirrhosis, due at least in part to increased renal ammonia synthesis. The latter effect is mediated in part by a transcellular potassium-hydrogen exchange.

* Potassium depletion may have two additional deleterious effects in patients with hypertension: it can raise the blood pressure by a mean of 5 to 7 mmHg (probably due in part to concurrent sodium retention); and it can increase the incidence of stroke, independent of other cardiovascular risk factors. On the other hand, potassium supplementation can lower the blood pressure by an average of 6/3 mmHg.

TREATMENT

All patients treated with a diuretic should be monitored for the development of hypokalemia during the first two to three weeks of therapy. In stable patients on a fixed dose of a diuretic (eg, for hypertension), potassium loss occurs only during the first two to three weeks of therapy before a new steady state is established.

Once a steady state is reached, further monitoring is not required, unless the diuretic dose is increased, extrarenal potassium losses increase, or dietary potassium intake is reduced. As an example, increased losses and decreased intake may be seen with gastroenteritis. In such patients, temporary cessation of diuretic therapy for a few days may be appropriate.

The best way to treat diuretic-induced hypokalemia is prevention by using the lowest effective dose. Not surprisingly, the risk of hypokalemia (as well as other diuretic-induced metabolic complications) is dose-dependent. Therapeutic issues vary with the underlying condition being treated.

Hypertension — In most hypertensive patients, 12.5 to 25 mg of hydrochlorothiazide (or its equivalent) produces as great a fall in blood pressure as higher doses, but a much smaller reduction in the serum potassium concentration.

The frequent lack of improved blood pressure control with higher diuretic doses may be related to activation of the renin-angiotensin-aldosterone system: angiotensin II is a potent vasoconstrictor that will tend to counteract the antihypertensive effect of more fluid loss, while hyperaldosteronism will enhance urinary potassium losses.

Low-dose thiazide therapy is not generally used in patients with resistant hypertension, underlying renal insufficiency, or an edematous state. Loop diuretics are preferred in the latter two settings. (See "Optimal dosage and side effects of loop diuretics" and see "Resistant hypertension").

Given the typically small reduction in serum potassium with low-dose thiazide therapy, prophylactic therapy to avoid hypokalemia is not warranted. If hypokalemia does occur, there are two main options: switch to another antihypertensive drug; or treat the hypokalemia with potassium chloride supplements (beginning with 40 meq/day) or with a potassium-sparing diuretic such as amiloride, triamterene, or spironolactone. Among the potassium-sparing diuretics, we prefer amiloride because it has the fewest side effects.

Potassium-sparing agents also spare magnesium [1,9,11] . This is a desirable effect since diuretic-induced magnesium depletion may be directly arrhythmogenic and may also cause hypokalemia that is refractory to potassium repletion alone.

Correction of hypokalemia has the added advantage of producing a small further reduction in blood pressure

Heart failure and cirrhosis — Prophylactic therapy to prevent hypokalemia is an important issue in patients with heart failure and cirrhosis:

* Among patients with heart failure, hypokalemia may precipitate serious arrhythmias. It is recommended that the serum potassium concentration be maintained between 4.0 and 5.0 meq/L. In addition, hyperaldosteronism itself appears to contribute to adverse cardiac events in patients with moderate to severe heart failure due to mineralocorticoid receptors in the heart and vasculature. In such patients, outcomes may be improved with a mineralocorticoid receptor antagonist (spironolactone or eplerenone) (show figure 5). Thus, patients who need chronic therapy for a below goal serum potassium concentration should be treated with a mineralocorticoid receptor antagonist rather than potassium supplements.

The data supporting the cardiac and vascular toxicity of hyperaldosteronism are discussed separately. (See "Use of diuretics in heart failure", section on Improved survival with aldosterone antagonism, and see "Clinical features of primary aldosteronism", section on Cardiovascular risk).

* Among patients with cirrhosis, hypokalemia can promote the development of hepatic encephalopathy, perhaps in part by increasing ammonia production. The serum potassium concentration should be maintained above 3.4 meq/L. Most patients with cirrhosis are already being treated with spironolactone, since it is part of the recommended diuretic regimen. (See "Initial therapy of ascites in patients with cirrhosis", section on Concerns with diuretic therapy and section on Diuretic regimen).

As mentioned above, potassium-sparing agents also spare magnesium [1,9,11] . This is a desirable effect since diuretic-induced magnesium depletion may be directly arrhythmogenic and may also cause hypokalemia that is refractory to potassium repletion alone. (See "Signs and symptoms of magnesium depletion").

PROPHYLAXIS

A separate issue from potassium replacement is the possible role of prophylactic potassium supplementation in patients with heart failure who need aggressive diuresis and have a borderline serum potassium concentration (eg, 4.0 to 4.2 meq/L since the goal is to maintain the serum potassium at a minimum of 4.0 meq/L). There are two approaches in such patients: more frequent monitoring, which we prefer, or prophylactic potassium supplementation.

MONITORING

After initiation of either potassium-sparing diuretics or potassium supplements, potassium levels must be monitored. As with the development of hypokalemia, the rise in the serum potassium concentration with a fixed dose of either potassium chloride or a potassium-sparing diuretic in a stable patient will generally be complete within the first two to three weeks of treatment. Ongoing periodic monitoring is required in patients with heart failure or cirrhosis, who may have progressive disease.

SUMMARY AND RECOMMENDATIONS

Hypokalemia is a relatively common problem with diuretic therapy, with the risk increasing at higher doses. Marked hypokalemia (serum potassium concentrations ≤2.5 to 3.0 meq/L) is uncommon, being described in fewer than 10 to 15 percent of patients receiving high doses of diuretics.

The development of hypokalemia is of greatest concern in patients with underlying heart failure or cirrhosis, as it may lead to arrhythmias and hepatic coma, respectively. In addition, it may lead to a modest elevation in blood pressure in hypertensive patients.

In patients with hypertension who develop diuretic-induced hypokalemia, either another agent can be used, or the hypokalemia can be treated with a potassium-sparing diuretic or potassium supplementation. If a potassium-sparing is chosen, we suggest amiloride, as it has the fewest side effects.

In patients with heart failure or cirrhosis who develop hypokalemia on diuretic therapy, therapy should include a mineralocorticoid receptor antagonist since these drugs are used for reasons other than hypokalemia:

* In patients with heart failure, we recommend a mineralocorticoid receptor antagonist (spironolactone or eplerenone) because of improved survival due in part to blockade of mineralocorticoid receptors in the heart and vasculature (Grade 1B).

Such benefits of mineralocorticoid receptor blockade have not been evaluated in patients with essential hypertension in whom hyperaldosteronism is not a typical feature. However, mineralocorticoid receptor blockers are important in patients with primary aldosteronism.

* We recommend a mineralocorticoid receptor antagonist (spironolactone or, if not tolerated, eplerenone) in patients with cirrhosis and ascites due to increased diuretic efficacy compared to amiloride (Grade 1B).

After initiation of potassium sparing agents or potassium supplements, potassium levels should be monitored, particularly during the first two to three weeks of treatment and after dose adjustments.

Diuretic-induced hypokalemia is best prevented by use of the lowest effective dose.

We suggest not routinely providing prophylactic therapy to prevent hypokalemia (Grade 2C). This is particularly true in patients with hypertension on low-dose thiazide therapy. Patients with heart failure who are undergoing a rapid diuresis require more frequent monitoring of the serum potassium concentration.

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