Renal Failure
Renal Failure is due to prerenal, intrarenal and postrenal conditions.
Acute Renal Failure is defined as the rapid breakdown of renal functioning which is the result of high levels of uraemic toxins in the cardiovascular system. Acute renal failure is often abbreviated to ARF in nursing and medical literature. These toxins are the waste products of the human body’s metabolic processes. The causes of these high levels toxins will be explored later. Acute Renal Failure is said to occur when the kidneys are unable to excrete the daily load of toxic metabolites in the urine.
Normal average urine production for the adult healthy individual is 0.5 ml/kg of body weight. Patients suffering from ARF are subdivided into two groups according to the amount of urine produced over a 24-hour period.
By definition both kidneys must be failing when ARF occurs. This is because even one normally functioning kidney is sufficient to maintain satisfactory blood filtering. Additionally, one new functioning kidney if successfully transplanted will be able to deal with the work load of the whole body.
In order to understand this article better, it may be helpful to revise the normal anatomy and physiology of the renal system.
Oliguric Patients: Produce less than 500 mls of urine in one day.
Nonoliguric Patients: Produce more than 500 mls of urine per day. Despite the fact that the amount of urine produced is satisfactory, the urine is of poor quality, and contains very little waste products.
Types of Renal Failure
Generally, renal failure is subdivided into three types according to the origin of the failure within the renal system of the patient’s body. The causes of renal failure are very diverse and we will explore these in the context of the Northern Territory.
- Pre Renal Failure
- Intrinsic Renal Failure
- Post Renal Failure
PRE-RENAL FAILURE (ARF)
Pre Renal (ARF) Failure is said to occur when there is inadequate blood circulation (perfusion) of blood vessels supplying the kidneys. In this situation the kidneys are unable to filter the blood of toxins adequately. This generally happens when a patient is critically ill and goes through a hypotensive state. This is a condition in which very low blood pressure occurs and perfusion of the renal glomerulus is not maintained. Often, in shock, multiple organ failure is common.
Dehydration: Dehydration is defined as a significant reduction in circulating water. It is caused by drastically reduced fluid intake, (consciously or unconsciously) or by excessive use of diuretics. The net effect of these conditions simply means that the body does not have sufficient volume of water. Dehydration occurs when the net fluid intake is less than output. Does this situation occur in the remote areas of Australia? Other causes of dehydration are acute and chronic diarrhoea, vomiting, fever, and excessive sweating. Mild dehydration causes fatigue, weakness and dizziness but severe dehydration causes renal failure and eventual death.
Heart failure: The usual management of heart failure dictates that the patient is kept slightly dehydrated. The slight dehydration and reduced perfusion of the kidneys is sufficient to cause pre renal failure. Is this condition common in Indigenous Australians? Discuss the social, environmental and historical causes for your answer. Why are patients in heart failure kept slightly dehydrated? Why is there reduced renal perfusion in the patient suffering from heart failure?
Patients with heart failure are kept slightly dehydrated because fluid build up in the lungs will cause shortness of breath and tissue hypoxia. How are such patients kept dehydrated?
Answer: Patients with heart failure are kept slightly dehydrated by the use of diuretics. One commonly used diuretic is frusemide (lasix).
Patients suffering from heart failure often have reduced blood flow (under perfusion) to the kidneys because the failing heart is unable to generate the pressure which is needed for adequate renal perfusion. This problem is exaggerated by the reduction in circulating fluid volume (hypo volumia).
Sepsis (Severe Infection): Sepsis is a medical emergency. It is condition due to the presence of real or suspected infection with two or more of the following conditions:
- Heart rate of more than 90 beats per minute.
- Body temperature of less than 36 degrees Centigrade or more than 38 degrees Centigrade.
- Respiratory rate of greater than 20 breaths per minute (hyperventilation)or a PaCO2 of less than 32 mm Hg. This will require blood gas analysis.
- White cell count of less than 4000 cell per cubic mm or more than 12000 cells per cubic mm or greater than 10% band forms ( immature white blood cells).
Severe sepsis reduces circulating fluid. Discuss the causes for this condition?
Severe blood loss is defined: as losing one fifth or more of the normal amount of blood of the human body. Such loss will cause hypovolemic shock. Severe blood loss will also cause a reduction in circulating fluid and a reduction in renal perfusion pressure which was discussed under the “dehydration”.
Pre existing atherosclerosis: (Prerenal ARF) Several pre-existing medical conditions such as atherosclerosis (Atheroma / fatty deposits in the arteries, resultant hardening of arteries) reduce blood flow to the kidneys. Reduced blood flow brings about pre renal ARF.
Idiopathic causes: Read the article at
med.ualberta.ca
Question: Discuss the causes of ARF in the Australian context.
Signs and Symptoms of ARF: A sign, by definition, is what we as nurses can see in a patient. An example of a sign is ankle oedema. Symptoms are what the patients tell us. An example of a symptom is pain.
A preponderance of patients may have the following signs and symptoms but these are non specific and can be present in other conditions. Accurate history taking and laboratory tests must be done to diagnose ARF.
- Dizziness: This is related to reduced circulating fluid.
- Dry mouth: Related to reduction of circulating fluid.
- Low blood pressure (hypotension): Due to lack of fluid and inability of heart to generate blood pressure which is normal for the patient’s age.
- Rapid heart rate: The tachycardia, increased heart rate, is produced by the heart’s attempts to compensate for the reduced circulating volume.
- Slack but leathery skin: This is the result of dehydration of the tissues of the body. When you pinch a fold of the skin and let go it will maintain it’s leathery shape for a while. Normal hydrated skin returns to normal shape the moment it is let go.
- Thirst: The thirst center in the brain is stimulated by the lack of water in the blood.
- Weight loss: 70 % of the human body is water. Weight loss will occur when circulating fluid is reduced.
As stated earlier urine output is usually low (oliguria) in patients with prerenal ARF. These patients may also have signs and symptoms of cardiac or hepatic disease.
Complications of ARF
Prerenal ARF causes patients to become critically ill. They are frequently admitted to acute care or intensive care units. Most of these patients have severe infections such as hepatitis or meloidosis. This sepsis results in decreased perfusion. As stated earlier, decreased perfusion leads to cardia, liver and renal failures. To learn more about the signs and symptoms of cardiac failure please visit the web site of The American Heart Association.
The main signs and symptoms of heart failure are:
- Shortness of breath, technically called dyspnea. This is associated with circulatory overload because the kidneys are unable to get rid of excess circulating fluid.
- Ankle oedema and pulmonary oedema are common. These are related to fluid retention in the tissues, particularly in dependent areas.
- Venous distension due to engorgement with excessive fluids.
Signs and Symptoms of hepatic (liver) failure include those listed below. For more information please visit
Healthtouch .
Confusion – leads to disorientation – stupor. The underlying patho physiology is of encephalopathy. During this condition the brain becomes more and more confused. This results in behavioral changes which are out of voluntary control of the patient. With time, the patient may go into a coma. Death is likely to follow.
Sweet, ammoniacal odor. Hepatic failure results in the accumulation of ammonia in the patients circulation. The ammoniacal smell is due to this ammonia. Elevated ammonia levels contribute to hepatic encephalopathy but the precise mechanism remains unclear.
Diagnosing ARF: Go to the website of the American Family Physician and read the article on Acute Renal Failure.
- For the purposes of accurate diagnosis and complete medical history must be taken
- This must be followed by a physical examination
- Blood must be sent to the laboratory. If it reveals a high BUN to Cr ratio (BUN:Cr > 20:1), along with abnormal urine chemistry then a diagnosis of ARF may be made.
- On the basis of the history and physical findings the physician must rule out post renal and intrinsic renal causes of ARF.
Treatment of ARF
There are many interventions to treat and manage Acute Renal Failure. All the interventions are aimed at improving renal perfusion. In many situations this will involve the treatment and management of the underlying condition (s). In general intensive care units the major issues are infection, heart and liver failures. This usually involves treating the infection, heart failure, or liver failure). Intravenous (IV) fluids are administered to most patients to treat dehydration.
Prognosis: In general, patients with prerenal ARF improve dramatically with intravenous fluids. Urine output increases and renal function improves.
INTRINSIC RENAL FAILURE (ARF)
Intrinsic renal failure is renal failure which is not caused by pre renal or post renal factors. In Intrinsic renal failure there is damage and injury with both kidneys. Approximately 40% of all renal failures are due to intrinsic factors. Some of the following are well known causes of intrinsic renal failure.
Vascular diseases – Diseases which affect the health and functioning of blood vessels.
- Glomerulonephritis and vasculitis: In these conditions the afferent, efferent and other arterioles / blood vessels are inflamed.
- Renal artery obstruction: The obstruction to the renal artery is the result of atherosclerosis or microscopic arterial thrombosis over a prolonged period of time.
- Low blood platelet and red blood cell counts resulting in tissue necrosis.
Thrombosis of the Renal vein resulting in obstruction and reduced blood flow.
Diseases of tubules and interstitial: (space between the cells) space.
- Amyloidosis (deposition of proteins in kidney tissues)
- Interstitial nephritis (associated with allergy or infection)
Acute tubular necrosis: The patho physiology of acute tubular necrosis is not clearly understood but it is generally believed that there are two main causes of tubular necrosis. Research shows that Ischemia and toxins cause close to 90 % of all intrinsic ARF. Both these conditions lead to Acute Tubular Necrosis, often abbreviated to ATN.
- Ischemia: Due to the lack of oxygenated blood. This occurs when there is hemorrhage (blood loss / bleeding), trauma, or sepsis from severe infections. These conditions may also occur in patients who are undergoing major cardiovascular surgery.
- Toxins: These are poisons which destroy the nephritic tubules. These can be sub categorized into endogenous or exogenous. Some toxins are the result of injury and others are created by electrolyte imbalances.
- Antibiotics like acyclovir, (roscarnet) used to treat infections
- Chemotherapeutic drugs (used to treat cancer, e.g., cisplatin, ifosfamide)
- Cyclosporine is medication which is used with other medications to prevent transplant rejection, most frequently for people who have received kidney, liver, and heart transplants
- Radiocontrast dyes used for x-ray imaging procedures
Some endogenous poisons which cause nephrotoxic ARF include the following:
- Rhabdomyolysis: During this condition toxins are released into the circulatory system which harm the kidneys. Generally, toxins are produced form destroyed muscle cells. An pigment that contains Iron, called myoglobin that exists in skeletal muscle enters the bloodstream after the muscle suffers damage. The primary muscle damage may be due to traumatic crush injury or from viral infections. Some may result from toxic reaction to prescription and nonprescription medications.
- Intoxication with alcohol, cocaine etc
- Seizures
- Traumatic crush injury, see Rhabdomyolysis above
- Hypercalcemia which is due high levels of calcium in the cardiovascular system. Most frequently this is caused by deposition of calcium in tissue. Sometimes it is due to vasoconstriction.
In conclusion it is fair to say that both ischemic and nephrotoxic ARF cause acute tubular necrosis (ATN). However, ATN is less pronounced in nephrotoxic ARF.
Allergic interstitial nephritis can be lead to ARF Causes, mainly:
- Antibiotics: Penicillins and Cephalosporins are most frequently implicated.
- Nonsteroidal anti-infmlammatory drugs like acetaminophen (Tylenol) and ibuprofen are also implicated.
Common signs and Symptoms
- Febrile states (pyrexia) associated with rash is a common feature. Joint pains, called arthralgia may be seen.
- Right, left or bilateral flank pain may be exhibited by some patients. Sometimes this is associated with obstruction of the renal artery or vein. Severe glomerulonephritis may be present.
- Mild to severe headaches associated with dizziness and confusion may be seen in the early stages of ARF. In the later stages, seizure-associated with malignant hypertension will occur.
- Decreased urinary output, urine output of less then 500 mls in an adult patient. Oedema and hypertension.
- Examination of the optic disc will reveal Papilledema
- Heart failure is sometimes seen
- Malignant hypertension associated with heart failure.
Frequent Complications of ARF
Metabolic acidosis is a frequent complication of ARF. Metabolic Acidosis is defined “impaired secretion of sodium and potassium and an imbalance of chloride”. This condition then leads to other mineral and electrolyte imbalances. Several other complications often occur during the course of intrinsic ARF. These are as follows:
- Elevated levels of serum potassium. (Hyperkalmia)
- Elevated levels of magnesium in serum. (Hypermagnemesia).
- Elevated levels of phosphates in serum. (Hyperphosphatemia)
- Decreased levels of calcium in serum. (Hypocalcemia)
- Circulatory overload. In this condition there is excess fluid in the circulatory system and the kidneys are unable to excrete that fluid.
- Uremia will occur. High levels of nitrogenous wastes stay in the circulatory blood. Nitrogenous wastes are the by products of protein metabolism.
Diagnosing Intrinsic ARF
The usual rules apply for diagnosing this condition. First an accurate history is taken. The signs and symptoms of the disease are noted. Then blood tests, urinalysis and imaging x-rays are performed.
Blood tests: Patients with intrinsic ARF are likely to show the following:
- High levels of serum creatinine due to renal ischemia, atheroembolism, or exposure to radiocontrast dye
- Severe and chronic anemia (low haemoglobin / red blood count). May indicate TTP-HUS.
- High levels of blood potassium. (Hyperkalemia),
- High levels of phosphorous. (hyperphosphatemia) and
- Low levels of blood calcium. (hypocalcemia) occurs mainly in rhabdomyolysis.
Urinalysis: Urinalysis will show many red and white cells in the urine. The level of sodium will generally be high. Failed filtering will result in proteinuria. Mild proteinuria suggests that renal failure is caused by injured tubules. Moderate proteinuria indicates glomerular injury. Heavy proteinuria indicates allergic interstitial nephritis.
Renal biopsy: This may be performed when laboratory test results are inconclusive or suggest more than one possible cause of intrinsic ARF.
Ultrasound: This examination is performed to rule out postrenal obstruction as the cause of the symptoms. Postrenal obstruction is obstruction in the urinary bladder or urethra.
Treatment of Intrinsic ARF
The main aims of treatment for intrinsic ARF are to resolve the underlying causes and manage the complications.
The specific aim in nephrotoxic ARF is the elimination of toxins. In ischemic ARF the main aim is to restore blood flow to the kidneys.
Acute glomerulonephritis and vasculitis are generally managed with glucocorticoids and plasmapheresis (plasma exchange).
In allergic interstitial nephritis, if the drug causing the condition is known it is discontinued. To manage the damage which has been caused the patient may be prescribed glucocortoids.
Most frequently, malignant hypertension is treated with ACE inhibitors. ACE inhibitors do not treat the underlying condition but help manage the blood pressure at accepted levels.
Treatment of Complications of Intrinsic ARF
- Circulatory overload is managed by salt and water restrictions
- Hyponatremia (low sodium level) in blood is managed with water restriction
- High level of potassium in the blood (hyperkalemia) is managed with dialysis, K+ restriction, and administration of Na bicarbonate
- Metabolic acidosis is managed with dialysis, dietary protein restriction and administration of sodium bicarbonate
- Hyperphosphatemia is managed by dietary restriction of phosphates
- Hypocalcemia is managed by the administration of calcium carbonate and calcium gluconate
- Hypermagnesemia is managed by the discontinuation of magnesium-containing antacids. Maalox is a classical example.
Common Indications for commencement of dialysis:
- Hyperkalemia: High levels of potassium are not compatible with life. Normal K is 3.5 to 4.5 mmols per liter. Hence dialysis is indicated.
- Circulatory overload occurs when the kidneys are unable to excrete the excess of consumed or metabolically produced water. When the kidneys become nonresponsive to diuretic treatment then dialysis is indicated.
- Severe acidosis, as defined above, which is nonresponsive to other treatments
- Severe uremia is not compatible with life. Hence dialysis is indicated.
Long term Prognosis: Mortality rates from Intrinsic Acute Renal Failure depend on the underlying causes of the disease. Approximately 33 percent of patients with this condition (acute toxin induced ARF) die. Approximately 66 percent of patients with intrinsic ARF (which is a complication of major cardiovascular) surgery also die. In conclusion, it is reasonable to state that the outlook is worst when there is oliguria in the patient. Lastly, the outlook for older clients with multiple organ failure is also not encouraging.
POSTRENAL FAILURE (ARF)
Postrenal ARF is the result of an acute obstruction to the outflow of urine from one or both kidneys. The obstruction results in back pressure in the functional units of the kidneys – the nephrons. As we already know the nephrons are the tubular filtering units which produce urine. The excessive back pressure of fluid ultimately causes the nephrons to stop functioning. The amount of renal failure generally is in a linear relationship to the degree and severity of obstruction. Postrenal ARF is prevalent in older patients (mostly males) who have enlarged prostate glands which obstruct to drainage of urine.
Common Causes of Postrenal ARF
There are many causes of postrenal ARF. Some of the common ones are listed below.
- Urinary bladder outlet obstruction. This is most commonly due to an enlarged prostate gland or bladder stones.
- Renal calculi in one or both ureters. Ureters are the small drainage tubes which drain urine from the kidneys to the urinary bladder.
- Grossly distended bladder. Most frequently due to a neurological disorder which results in an inability of the bladder to empty.
- Sometimes the end channels of the renal nephrons become obstructed. When this happens postrenal ARF is likely to result.
- Renal injuries: These may be due to motor vehicle or sports injuries
- Formation of fibrous tissue behind the peritoneum – Retroperitoneal fibrosis. In normal health these fibres lines the abdominal cavity. Their function is to hold the contents of the abdomen in place.
Signs and Symptoms of Postrenal ARF
Flank pain is the most common symptom. However, it varies in severity and location according to the type of obstruction. Other signs and symptoms of postrenal ARF are as follows:
- Difficult urination
- Distended bladder
- Generalized oedema: fluid retention with resultant swelling due to accumulation of fluid in the intracellular spaces
- Underlying Hypertension or high blood pressure particularly when under treated or not treated
- Pain in the either flank, lower abdomen, groin, and genitalia
- Hematuria; presence of frank/ visible blood in the urine
How to diagnose Postrenal ARF
Diagnosis of postrenal ARF should be initiated with a complete physical examination and medical history. Insertion of a foley catheter will reveal a grossly enlarged urinary bladder with a capacity of 2 to 3 liters. For details on how to insert a foley catheter you may visit
healthmad.com
.
CT or CTT scans of the kidneys can provide useful information about the kidneys, ureters and bladder.
Ultrasounds are the usual tests of choice for diagnosing postrenal ARF. If the kidneys show signs of hydronephros (stretched and dilated renal pelvis), beyond normal dimensions a diagnosis of postrenal ARF can usually be made with certainty.
Treatment & Management
The relief of obstruction is the main aim of treatment in this situation. When the underlying problem is bladder outlet obstruction then the problem needs to be corrected. In older male patients the problem is usually an enlarged prostate. This condition is also knows as benign prostate hyperplasia (BHP). Learn more about BHP at healthmad.com .
Insertion of a Foley or supra pubic catheter will usually relieve the obstruction temporarily. IF the underlying cause is bilateral renal calculi in one or both ureters then the calculi must be removed surgically or by other means. In some instances the insertion of bypass drainage tubes to drain urine from the kidneys through an opening in the skin may be necessary. These are called percutaneous nephrostomy tubes.
Complications of postrenal ARF
Treatment of urinary tract obstruction is often associated with a variety of undesired outcomes. These include, but are not limited to the following:
Haematuria: This may occur when a catheter is passed into the bladder. This is often the result of the sudden decrease in the internal bladder pressure. This decrease causes the bladder veins to bleed. Some studies show that slow decompression of the bladder does not prevent gross haematuria.
Reflex hypotension: Is another which condition which may occur, sometimes. This is the result of sudden stimulation of the vagus nerve during the process of catheter insertion.
Postobstructive diuresis: Occurs in some patients. This is a rare condition during which there is high urine output. Initially, it may be in excess of 500 to 1000 mls. each hour. This occurs when the obstruction is removed. In this situation it may be necessary to give IV fluids in large amounts to prevent severe dehydration and associated complications.
Prognosis: Long Term. The rate and amount of recovery is largely determined by the duration and severity of underlying obstructive disease. Most of the expected recovery will occur within 7 to 14 days after the obstruction has been removed. A few patients may require short-term dialysis until their renal function recovers. Hemodialysis involves removal of waste products from the blood via mechanical filtration outside of the body. This is a highly specialized skill which must be done in a hospital or a specialized renal unit.
Some patients with postrenal ARF will develop irreversible tubular defects with the following symptoms.
- Hyperkalemia: Elevated blood potassium.
- Metabolic acidosis: Elevated level of chlorides in the body.
- Polyuria: Excessive amounts of urine.
|
Summary of Laboratory Results: Acute and Chronic Renal Failure |
|||||
|
Acute renal Failure (ARF) |
CR Failure | ||||
| Prerenal |
I n t r a r e n a l |
Postrenal | |||
| History | GI, GU, skin, hypovolumia, severe blood loss, 3rd. spacing. | Toxins, Drugs, O&B complica- tions. | Allergy to drug (s) | Various causes,
Age dependent. |
Impaired management of DM
& HTN. |
| Manifestation. | Reduced BP related to volume depletion | No S&S, some exceptions. | Elevated Temp.,
Possible Rash. |
Flank pain, bladder distension, renal hypertrophy, neoplasm | Itching, anaemia,
Echogenic kidney (s), bone disorder |
| BUN&
S.Cr |
>20 | <20 | 10 to 15 | 10 to 15 | 10 to 20 |
| UNa (mEq/L) | <20 | >20 | >40 | >40 | >20 to 40, may be variable. |
| Uosm
(mOsm/kg H2O) |
>500 | <350 | <350 | <350 | Variable |
| UCr & SCR | >40 | <20 | <20 | <20 | Variable |
| FENa
(%) |
<1 | >1 | >1 | >1 | Variable |
| Proteinuria | None to trace | Mild to moderate | Mild to moderate | None to trace | Trace to moderate |
| Sediment (s) | Normal to few cast cells. | Pigmented casts may be visible | Esinophils
WBCs & RBCs |
RBC, WBC, crystals | Variable |
Table: Differences in Lab. Results for the three stages of ARF’s.
Disclaimer: This article is for educational purposes only. It does not discuss all possible ramifications of ARF for all possible patient situations and conditions. It must not be used for treatment and management of ARF. Only medical practitioners are authorized to treat and manage ARF.
Key words used in this article: hyperkalemia, hypokalemia, metabolic acidosis, polyuria. Prerenal ARF, Intrarenal ARF, postrenal ARF, hemodialysis, dehydration, postobstructive diuresis, diuresis, vagus nerve, reflex hypotension, atheroembolism, oliguria, sepsis, toxins, flank pain, hydronephrosis, hypo volumia, circulatory overload, hyponatremia, hypernatremia, multiple organ failure, traumatic crush injury, Rhabdomyolysis, hyperphosphatemia, restriction of phosphates, hypocalcemia, calcium carbonate, calcium gluconate. hypermagnesemia, percutaneous nephrostomy.
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