Definition:
Renal failure is failure of renal excretory function due to decreased glomerular filtration rate and may be accompanied by failure of:
· EPO production
· Vitamin D hydroxylation
· Regulation of acid-base
· Regulation of salt-water balance and blood pressure
Acute renal failure is abrupt deterioration of this function and may be reversible.
It leads to uraemia and/or oliguria and is life-threatening due to the subsequent biochemical malfunctions.
Sources: Kumar and Clarke
From Angela
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Causes of Renal Failure
Acute renal failure, also know as Acute Tubular Necrosis, is a temporary condition where kidney function declines rapidly and results in reduced excretion of nitrogenous waste products of which urea is most commonly measured. Causes include severe blood loss, shock, kidney stones and tumours, sepis or kidney damage due to disease or toxic substances. Therefore the kidneys are unable to maintain proper balance of water and chemicals. Uraemia can be:
1)Prerenal – In this condition, there is impaired perfusion of the kidneys with blood. It results from Hypovolemia, Hypotension, effects of drugs (NSAID’s, ACE Inhibitors) impaired cardiac pump efficiency or vascular disease limiting renal blood flow. Hypotension, weak rapid pulse and a low jugular venous pressure suggests that uraemia is prerenal. All causes lead to parenchymal kidney damage and hence acute renal failure. The condition improves once normal renal perfusion is restored.
2)Renal – It is an inherent problem in the kidney itself. It can be an autoimmune condition where the kidneys are attacked by the body’s own defence mechanism. It can also be as a result of Renal Parenchymal disease whose causes include Glomerulonephritis (inflammation in the kidneys resulting in damage), accelerated hypertension and cholesterol embolism.
3)Post renal – This condition results from obstruction of the urinary tract at any point from calyces (collecting structures in the kidney) to external urethral orifice. Eg. Blood clot, Bladder tumour, Tumour of renal pelvis or ureter and congenital urethral valve.
References:
1)Kumar and Clark
2http://www.hmc.psu.edu/healthinfo/a/acuterenalfailure.htm
3http://mayoresearch.mayo.edu/mayo/research/nephrology/parenchymal.cfm
Signs and Symptoms of Acute Renal Failure
Signs:
Generalized swelling caused by fluid retention
Auscultation: heart murmur
Crackles in lungs
pericarditis (inflammation of lining of the heart)
- due to fluid build up
Symptoms:
Oliguria: Decreased production of urine
Anuria: urine production has ceased
Nocturia:Excessive urination at night
Peripheral Oedema:abnormal build up of fluid in ankles, feet and legs
Paresthesias: decreased sensation, especially in the hands and feet
Decreased appetite
Metallic taste in mouth
Persistent hiccups
Changes in mood:agitation, drowsiness, lethargy, delirium or confusion, trouble paying attention, hallucinations
Slow, sluggish movements
Hand tremor
Nausea or vomiting
Bruising easily
Prolonged bleeding
Nose bleeds
Bloody stools
Flank pain (between ribs and hips)
Fatigue
Breath odor
High blood pressure
References:Medline Plus Medical Encyclopaedia, ‘Acute Kidney failure’, http://www.nlm.nih.gov/medlineplus/ency/article/000501.htm
Renal Replacement Therapy
Renal replacement therapy involves replacing the normal function of the kidneys in patients with renal failure.
Indications for RRT:
Acute
- Hyperkalaemia
- Metabolic acidosis
- Fluid overload (seen as peripheral oedema)
- Uremic pericarditis
- Non-renal causes (eg poisoning)
Chronic
- Symptomatic renal failure
- Low glomerular filtration rate
- Failure of medications
There are 3 main types of RRT:
Haemodialysis
Peritoneal Dialysis
Haemofiltration
Haemodialysis:
Haemodialysis involves the diffusion of solutes across a semi-permeable membrane. Blood is taken from the patient and passed through the haemodialysis machine. In this machine, a semi-permeable membrane separates the blood from dialysate, a sterile solution containing electrolytes and glucose. Waste materials in the blood diffuse into the dialysate down their concentration gradients, thus cleaning the blood. This also causes water to flow out due to osmosis. Often patients with renal failure have fluid retention problems, so this is beneficial, but the amount of water excreted can be controlled by the concentration of glucose in the dialysate. Na and Cl are also present in the dialysate in isotonic concentrations to prevent salt loss, and bicarbonate may be included if the patient has acidosis. Heparin (or another anticoagulant) is also used to prevent blood from clotting in the machine.
Access sites for the blood include venous catheters, arteriovenous fistulas and arteriovenous grafts. All have their advantages and disadvantages, but for most patients AV fistulas are the preferred option. This is where an artery and a vein (commonly in the arm) are surgically grafted together, meaning that there is some blood flow bypassing the capillary beds. This leads to more efficient flow of blood into the dialysis machine. Obviously the most common side effect associated with these access sites is infection.
Haemodialysis times are determined by a nephrologist, with the average being 3-4 hours, 3 times a week. Because this is performed at special out-patient clinics, this is a considerable inconvenience to patients.
Peritoneal Dialysis:
The principles of peritoneal dialysis are quite similar to haemodialysis, but in this case the peritoneum acts as a natural semi-permeable membrane. A catheter is inserted into the abdominal cavity, and the dialysate is introduced directly, then after several hours it is drained before beginning the procedure again. It can be done by the patient themselves at home, and takes only 30 minutes with a minimum of equipment. This means that they have much more freedom than those on haemodialysis. However, the risk of infection is higher, and it requires a high level of patient motivation, plus a sufficient level of skill and commitment to infection prevention. Also, over time the peritoneum can begin to lose its permeability, meaning that patients may eventually have to move on to haemodialysis.
Haemofiltration:
Haemofiltration is similar to dialysis in that it involves filtration across a semi-permeable membrane, except that it is hydrostatic pressure that drives the filtration, not diffusion. Fluid and waste solutes in the blood are forced across the membrane and discarded, and isotonic fluid is re-introduced into the blood to prevent hypovolaemia. This fluid again often has bicarbonate to correct acidosis. Haemofiltration can be given either intermittently or continuously, and is used almost exclusively in ICU.
Kidney Transplantation:
Kidney transplants are only used in end-stage renal disease, and are not given for acute renal failure.
References
R. Sinert, P. Peacock; "Renal Failure, Acute"; eMedicine, Mary 10 2006
"Treatment Methods for Kidney Failure", National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), from http://kidney.niddk.nih.gov/kudiseases/pubs/kidneyfailure/index.htm
Splenectomy
Function of the Spleen:
- Foetal erythopoeisis (may resume this role in extreme anaemia)
- Monitoring of blood for antigens
- Site of phagocytosis of old erythrocytes
- Can compensate for hypervolaemia by transferring plasma from bloodstream to lymphatics
A person can live without a spleen, but will be more vulnerable to infections (especially from encapsulated organisms)
Splenectomy:
If splenic haemorrhage is suspected, rapid surgical correction is indicated. Stable patients may have a CT scan to confirm this, but unstable patients will usually undergo exploratory laparotomy instead, as this allows for treatment at the same time. If it is indeed the spleen that is ruptured, it will be repaired if possible, but most often it must be removed.
Stages of a splenectomy (during a laparotomy):
- Midline abdominal incision
- Dissection of gastrosplenic and splenorenal ligaments
- The spleen is rotated medially (to expose the splenic hilum)
- The splenic artery and vein are ligated
- The gastric vessels are also ligated and carefully separated from the spleen
- The spleen can now be removed
- Care must be taken during the procedure that the tail of the pancreas is not damaged (as it is often intimately positioned near the splenic hilum)
There are no contraindications to this surgery, as it is life-saving.
Complications include bleeding from the splenic or gastric vessels, and infection. Infection is a risk for any surgery, but especially so for splenectomy as it is an organ of the immune system. Patients are vaccinated against pneumococcus spp, haemophilus spp and meningococcus spp. If the surgery is planned, these vaccinations will be given pre-operatively, but as most splenectomise are due to trauma, the vaccines are usually given upon discharge.
References
Saladin; "Anatomy & Physiology (3rd Ed)"; 2004
H. Bjerke, J. Bjerke; "Splenic Rupure"; July 27 2006, from http://www.emedicine.com/med/topic2792.htm
Complications of Chronic Renal Failure
Diabetes Mellitus
Anaemia
- Erythropoietin deficiency
- Bone marrow toxins retained in renal failure
- Haematinic deficiency – iron, vitamin B12, folate
- Increased red cell destruction
- Abnormal red cell membranes causing increased osmotic fragility
- Increase blood loss – loss during haemodialysis
Bone Disease: Renal Osteodystrophy
- Reduced activation of vitamin D receptors in the parathyroid glands leads to increased release of parathyroid hormone.
- Renal failure also results in gut calcium malabsorption
- Phosphate retention owing to reduced excretion by the kidneys also indirectly lowers calcium
Skin Disease
Pruritus (itching) is common in chronic renal failure. This is due to retention of nitrogenous waste products of protein catabolism and iron deficiency.
Gastrointestinal Complications
- Decreased gastric emptying and increased risk of reflux oesophagitis
- Increase risk of peptic ulceration
- Increased risk of acute pancreatitis
- Constipation
Metabolic Abnormalities
- Gout
- Lipid metabolism abnormalities
Endocrine Abnormalities
Muscle Dysfunction
Uraemia (A toxic condition resulting from renal failure, when kidney function is compromised and urea, a waste product normally excreted in the urine, is retained in the blood) appears to interfere with muscle energy metabolism, but the mechanism is uncertain.
Nervous System
Central Nervous System
- Severe uraemia causes depressed cerebral function and decreased seizure threshold.
Autonomic Nervous System
- Increased circulation catecholamine levels associated with down regulation of alpha receptors.
- Impaired baroreceptor sensitivity
- Impaired efferent vagal function
Cardiovascular Disease
- Myocardial Infarction
- Hypertension
- Cardiac Failure
- Stroke
References:
Kumar and Clark
Medline: End Stage Renal Failure http://www.nlm.nih.gov/medlineplus/ency/article/000500.htm
Prognosis of splenectomy
Many, indeed most, people who do not have a spleen (asplenia) live perfectly normal lives without any clinical side effects at all. However the absence of a spleen may occasionally have consequences which merit further consideration.
1. The effects of losing the spleen on immunity:
- the most important consideration
- the spleen traps the cells infected by bacteria in one place and allows a more efficient attack by white blood cells
- loss of the spleen may result in impaired defence against bacteria
- For this reason all people without a spleen are advised to seek medical advice at an early stage if any infection occurs
- patients are recommended taking antibiotics (usually penicillin) on a twice daily basis after splenectomy to mop up these bacteria before the white cells are asked to deal with them
- It is also advisable that they are vaccinated (refer Shane's post), the ideal time to receive these vaccines is at least one week before the operation.
2. The effects of losing the spleen on platelet function:
-They are normally produced by the bone marrow and survive for up to two weeks when, if not required, are removed and replaced by fresh platelets from the bone marrow. The spleen is the most important organ in this removal process with some help from the liver.
-Loss of the spleen frequently results in a rise in the platelet count in the blood
-may result in the blood having too great a tendency to clot and the worry is that this could predispose to the development of strokes or heart attacks.
-To reduce this risk therefore it is sometimes necessary to advise people at risk of these complications to take daily aspirin tablets after the spleen has been removed.
3. The effects of losing the spleen on red cells:
- Red cells (erythrocytes) are produced by the bone marrow and live approximately four months before they decompose and their components are recycled.
- spleen aids this process by fragmenting the dying cells as they reach the natural end of their lifecycle
- However if one examines a blood film under a microscope after the spleen has been removed old cells may frequently be seen
- This is rarely a clinical problem.
reference:
http://groups.msn.com/MrBasilAmmori/laparoscopicsplenectomy.msnw
Function of the Kidney
Homeostasis
Hormone Secretion:
The kidney is responsible for the secretion of a number of hormones, but particularly three key components of homeostasis; renin, calcitriol and erythropoietin. Renin is released in response to high K+ levels or low Na+ levels, starting off the renin-angiotensin system. Calcitriol is produced from vitamin D and promotes reabsorption of calcium from the filtrate and absorption in the gut, in response to hypocalcemia, and is thus important in calcium homeostasis. Erythropoietin facilitates the production of erythrocytes.
Filtration and Excretion:
When amino acids are broken down in the body they produce small nitrogen-containing compounds known as nitrogenous wastes, roughly 50% of which is urea. Other nitrogenous wastes include creatinine and uric acid. These wastes circulate through the blood plasma until filtered and excreted by the kidney, without which they would accumulate in amounts toxic to the body. The kidney is also responsible for excreting other toxic substances into its filtrate such as penicillin, aspirin, various other drugs, catecholamines and bile acids.
Blood Pressure/Volume:
As described, the kidney releases renin, starting the renin-angiotensin system. This increases plasma volume, thereby increasing blood pressure.
Electrolyte Balance:
During the course of urine formation the kidney is responsible for ensuring the reabsorption of essential electrolytes such as sodium and phosphates and potassium in the concentrations needed for the body, or otherwise decreasing levels of these electrolytes by not reabsorbing them when levels are too high. This occurs mainly by secondary active transport along the proximal convoluted tubule. Sodium levels are low in the cells of the PCT so sodium diffuses in, while various co-transport proteins use this diffusion to transport various other molecules and electrolytes out of the filtrate. This is known as secondary active transport because it is an active transport mechanism that transports the sodium out of these cells (and potassium in), thereby keeping the concentration of sodium in these cells low. By this mechanism the fluid cavities of the body are maintained at a particular osmolarity. However the main mechanism of sodium balance actually occurs in the DCT, where receptors to aldosterone change the amount of sodium reabsorbed. This is also the site where water levels are determined by the hormone ADH. Stimulation of V2 receptors by ADH produces aquaporins which increases the amount of water reabsorbed, thereby controlling water level in the body.
pH Levels:
The kidney is able to partially regulate body pH by secreting H+ ions into the filtrate. This reacts with the bicarbonate ions (which have been filtrated out of the blood, but cannot be reabsorbed) in the filtrate to form carbonic acid, which dissociates into CO2 and water and is taken up by the tubular cells. Here it may reform H+ and bicarbonate ions, where the bicarbonate ions are taken back into the blood while the H+ ions may be reused in the cycle. By this mechanism, if there is more bicarbonate ions then H+ ions in the blood (alkaline) and thus the filtrate, then some won’t be reabsorbed and the level of bicarbonate in the blood will decrease lowering the pH. If there are less bicarbonate ions then H+ ions (acidic blood), then not all the H+ will react and that will be excreted in the urine and the pH will increase.
By Robb
References:
Saladin
Guyton and Hall
Junqueira, Basic Histology, McGraw Hill
Incidence of Renal Failure
Kidney failure rates were approximately 5 times higher for the indigenous population in Australia 2000-02 (Australia’s Health 2004, AIHW)
11,601 people were hospitalised for kidney failure in Australia 2001-02 (Australia’s Health 2004, AIHW)
The incidence of ESKD (End Stage Kidney Disease) below the age of 45 was stable between 1981 and 2002 (about 2 cases per 100,000) but for the age group 45-64 the incidence increased by 50% (from 10 to 15 per 100,000 population). During this period, incidence in the age group 65-74 increased ninefold (from 4 to 36 per 100,000). For the oldest age group (75 and above), the reported incidence of ESKD, low until 1992, was 30 per 100,000 in 2002 (Figure 9). The increasing prevalence of diabetes is a major contributor to this rise in ESKD incidence.
References
http://www.wrongdiagnosis.com/k/kidney_failure/stats.htm
http://www.aihw.gov.au/publications/aus/ah04/ah04-050222.pdf
GENERAL MEDICAL MANAGEMENT OF ACUTE RENAL FAILURE
- Monitor pulse, BP, CVP and urine output hourly. Also daily fluid balance and weight.
//Correct volume depletion with IV fluid – colloid, saline or blood (but may result in fluid overload)
//If septic, treat with antibiotics
//Check and adjust doses of any drugs taken (if renally excreted)
//Ensure normal calorie intake
//Urinary catheter placement (treats any urinary obstruction problems while measuring urine output)
MANAGEMENT OF COMPLICATIONS
//Hyperkalaemia (may cause arrthymias or cardiac arrest):
- IV calcium (cardioprotective)
- IV insulin + glucose (Insulin stimulates cellular uptake of K+, lowering serum K+)
- Haemodialysis or haemofiltration if persistent.
//Fluid overload, e.g. pulmonary oedema
- IV diuretics, e.g. frusemide
- Renal vascular vasodilators, e.g. morphine, dopamine
Reference: Emedicine - Acute Renal Failure article; http://www.emedicine.com/emerg/topic500.htm
Investigations for Acute Renal Failure
Acute or Chronic?
• Depends on history, duration of symptoms and previous urinalysis or measurements of renal function.
• Rapid rate of change of serum urea and creatinine suggests acute renal failure.
• Ultrasound assessment of kidney echogenicity and size; small kidneys indicate chronic (although kidney may remain normal in size in diabetes or amyloidosis)while normal looking kidneys indicate acute uraemia.
Prerenal, renal or postrenal?
• Urethral catheterization or flushing of existing catheter rules out bladder outflow obstruction. Renal Ultrasonography of upper urinary tract with absence of dilatation also rules out urinary tract obstruction.
• Assessment of the patient’s volume of urine and central venous pressure (CVP) measurement to distinguish Prerenal or renal causes. If volume is low, appropriate corrective measures should be done but if there’s no diuresis after that, acute intrinsic renal failure is present.
Other Investigations:
• Urinalysis, Urine Microscopy (red cells or red cell casts-glomerulonephritis) and urine culture.
• Measurement of serum urea, electrolytes, creatinine, calcium, phosphate, albumin, alkaline phosphatise and urate concentrations (FBE).
• Full blood count and peripheral blood film examination.
• Testing of urine for free haemoglobin and myoglobin.
• Coagulation studies.
• Blood cultures.
• Measurements of nephrotoxic drug blood levels.
• ECG:
- peaked T waves, PR prolongation and QRS widening (hyperkalemia-impaired renal potassium excretion)
- long QT segment (hypocalcemia)
References:
Kumar and Clark p. 640
Current Medical Diagnosis & Treatment p. 868
Dwinnell B.G & Anderson R.J “Diagnostic Evaluation of the patient with Acute Renal Failure” Viewed on: 25th April 2007. Available from: http://www.kidneyatlas.org/book1/adk1_12.pdf
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