Factors Affecting Kidney Function

Factors Affecting Kidney FunctionKidney Diseases and exterminate stage nephritic sorrow be not isolated to affecting just the kidney. any organs ar moved(p) by the disruption finished Kidney unsoundness and similarly opposite organs leave alone in any case affect the kidney and how it functions. The undermentioned five unsoundnesss show the impact they acquire on the kidney, its function and pathophysiology.2. human immunodeficiency virus/acquired immune deficiency syndromeRenal complications in patients with human immunodeficiency virus/AIDS rear be every as a result of the long-term repetition of, or simultaneous infections in an immune suppressed patient or as a result of the many drugs (nephrotoxins) use to treat the HIV/AIDS virus. The exact role that the HI-Virus plays in the pathology of the kidney is still contr oversial (James, 20051632-1633).There are a number of kidney diseases identified by means of biopsies associated with HIV, the most preponderant o ne be HIV-associated Nephropathy. Others are Mesangial Glomerulonephritis where immune deposits are seen, to a lesser degree in any case minimal change disease, TTP/HUS, Amyloidosis and Lymphoma (Dolin, 20081257).It was shown that the type of nephropathy was also clearly defined by race, much(prenominal) being that people of drab African origin predominantly showed HIV-associated nephropathy whereas in other racial groups immune complexes played the major role (James, 20051632-1633).In a take in finished by Tygerberg hospital in conjunction with Stellenbosch university it has shown that 54% of biopsies done on Black HIV positive patients show HIV nephropathies, in the USA this figure shows that it is the 3rd most roughhewn cause of end stage renal disaster (http//en.wikipedia.org/wiki/HIV-associated_nephropathy accessed 19/03/2011).In HIV-associated nephropathy thither is sclerosis of the glomerular apparatus as hygienic as microcystic tubulointerstitial disease which is de fined by the enlargement of the tubules with protein deposits in the tubular space as well as oedema in the surrounding tissue, fibrosis and inflammation (Dolin, 20081257).Where kidney booking is collectable to immune complex deposits the entire nephron is involved this can be as a direct result of infection from the virus or alternatively callable to the release of cytokines when first infected with HIV (http//en.wikipedia.org/wiki/HIV-associated_nephropathy accessed 19/03/2011). discourse sorts include transplantation, which can however, pose problems with regard to medical specialty interactions between antiretroviral drugs and immunosuppressants, furthermore a high rate of rejection as well as a high guess of cardiovascular disease business office transplant are a problem (Trullas in press)Treatment consists of slowing the act to ESKD and treating the HIV infection with antiretroviral drugs, further treatment with Angiotensin Converting Enzyme (ACE inhibitors) and angio tensin receptor blockers are used to treat hypertension, possibly immunosuppressant drugs or steroids and dialysis if kidney disaster progresses to inveterate (Greenberg, 2009254)3. MalariaThere are four types of malaria parasites the one that is in general cognise to show manifestations in other organs including the kidney is Plasmodium falciparum. There are over 500 million people infected with this parasite intercontinental with an annual death rate of between 1-3 million.There are over 100 countries worldwide in which malaria is prevalent and many of these countries have account a 0.57- 60% vivid renal affliction as a result of malaria. It has also shown that the stabbing renal trouble associated with malaria is more mutual in adults than children in the tropics where transmission of malaria is low or hazardous and where symptomatic disease occurs at all ages (Idonije, 20114-7)Acute renal failure occurs in a very small percentage of the cases infected, however the d eath rate rate can be as high as 45%. (Saroj, 2008395)The exact pathophysiology of Malarial Acute Renal Failure is not cognise scarce there are many theories as to how the kidney is affected, namely through obstruction and adherence of the vascular space by disease affected and thus altered erythrocytes, this is known as erythrocyte sequestration. Further, immune complexes may be responsible for changes in the glomerular and tubular physiology.Dehydration due to sweating, vomiting and trim fluid stirring can consume to tamed perfusion of the kidney with ischemia resulting in acute kidney failure.Pulmonary oedema, acute respiratory sorrow syndrome and anaemia are all factors that may complicate the malarial acute renal failure.Treatment options include the identification of the intricacy of the kidney early on which may be difficult in particular in home base treatment in the rural environment, renal switch overment therapy (haemodialysis or peritoneal dialysis), anti ma larial drugs, intravenous fluid replacement (although this may lead to pulmonary oedema and must be closely monitored), diuretics which may reduce the time the patient requires dialysis, possible communication channel transfusion to help replace fluids as well as answer with the malaria induced anaemia and the turning a modality of nephrotoxic drugs (Das, 200883-97).Mortality of patients increases with high Creatine levels, oliguria/anuria, anaemia CNS involvement and late referral to a tertiary care center for early commencement of treatment, age plays no role in the mortality of these patients (Kanodia, 20101088-1091).4. HUS/TTPThere are three reasons for thrombocytopenia namely due to platelet destruction as in Thrombotic Thrombocytopenic Purpura (TTP) and Haemolytic Uremic Syndrome (HUS), failure of platelet yield as in malignancies and platelet sequestration (Underwood, 2009585)TTP and HUS are some(prenominal) thrombotic microangiopathies and both are characterised by the deposition of c disperses in the small vessels of various organs, amongst these being the Kidney. There is a large clinical overlap between the ii (Underwood, 2009670).HUS is an acute disorder often following a haemorrhagic or diarrhoeal illness. It is characterised by microangiopathic haemolytic anaemia, which is caused due to an increase in fibrin in the vessels and this fibrin network damages the erythrocytes causing anaemia. It has been established that HUS is associated with viral and bacterial infections especially in children (McCance, 20101408).Both HUS and TTP are linked to pregnancy cerebrate acute kidney failure only when it is a rare occurrence. If they occur then(prenominal) HUS loosely occurs postpartum whereas TTP is linked to pre-eclampsia and occurs pre delivery (Greenberg, 2009410).The toxin released from a bacterium much(prenominal) as E. coli causes inflammation when it attaches to the wall of the intestine and from here enters the vascular system. It find s its way to the kidney where it causes damage both in the glomerular and tubular system through thrombosis, and inflammation and thus kidney failure. This infection may also cause fever, hypertension, intellectual and pulmonary oedema, congestive heart failure and seizures (Lerma, 2009289).TTP on the other pop off is caused by blockage of the small vessels through the accumulation of platelets causing vascular lesions in the central nervous system, heart and kidney causing organ failure or malfunction (Underwood 2009671).There are two types of TTP, one is chronic relapsing TTP which is rare and the other is idiopathic relapsing TTP. This is a lot more severe in its course and can be pitch-dark within 3 months if left untreated (McCance, 20101046).Treatment for diarrhoeal related HUS is generally supportive, fluid-electrolyte replacement, blood transfusion and dialysis if needed. Recovery rate is high but there is a 3-5% mortality rate during the acute phase (DAgati, 2005498)Glome rular involvement HUS has a better prognosis than HUS with a high vascular involvement.Compared to HUS, the TTP has less haemolysis and milder renal impairment but shows more neurologic symptoms such as confusion, headache and motor and sensory defects.Treatment for TTP takes the form of plasma exchange with fresh frozen plasma. Since the implementation of this therapy form the mortality rate has dropped by approximately 25% but with severe renal involvement it still has a poor prognosis. It may re-occur in 25% of the patients who have been successfully treated (DAgati, 2005511).5. HELLP SyndromeHELLP Syndrome is an acronym for Haemolysis, Elevated Liver enzymes, and Low Platelets and is generally found in large(predicate) woman who have gear uped preeclampsia or eclampsia (Gould, 2006120). Symptoms are Microangiopathic haemolytic anaemia, elevated liver enzymes are due to obstruction of the hepatic vessels by fibrin deposits and the low platelets are the result of either increas ed use of or the destruction of platelets (Counts, 2008168).HELLP Syndrome may only develop during labour and as with preeclampsia the best cure is the delivery of the baby. difficult bleeding is un probable unless platelet counts are very low (below 50 000/mm3). Severe thrombocytopenia or rupture of a subcapsular liver hematoma can both be life threatening (Ratcliffe, 2008493)Many signs and symptoms such as jaundice, hematuria, GIT bleeds, gum bleeds can be seen in pregnant woman which are related to HELLP but could be mistaken for other diseases such as Hepatitis, ulcers, kidney stones, glomerulonephritis, TTP or HUS so a full blood count is essential to differentiate HELLP from other diseases (Queenan, 2007275)HELLP Syndrome is one of the Thrombotic Microangiopathies as is TTP and HUS but as it is a result of preeclampsia it only occurs during pregnancy and then usually only in the third trimester. Preeclampsia is more common than TTP/HUS during pregnancy but with a lower risk of renal failure unless the case is a severe one.HELLP syndrome shows mild disseminated intravascular coagulation (DIC) which is characterised by undisciplined coagulation, increase in bleeding time and liver enzymes (Greenberg, 2009410)It can be potentially fatal to the expectant mother, decrease perfusion of placenta thus threatening the fetus (Counts, 2008168) with a mortality rate of up to 24% for the mother and 7.7 60% to the unborn due to intrauterine asphyxia, placenta detachment or extreme prematurity (Feehally, 2007350).In some instances symptoms do not improve after hand over but generally the best therapy is the delivery of the baby. Corticosteroids may be used to help hasten the recovery and reduce the need for blood products (Feehally, 2007350). Treatment is generally symptomatic the stasis of any bleeding, blood products if a significant meter of blood was helpless or is still likely to be lost without intervention, and the same applies for FFP. A cryoprecipitate may be given if the fibrinogen levels are low (for example Factor VIII from frozen blood) and fibrinolysis inhibitors may be considered in some patients (McPhee, 2009474-475).6. RhabdomyolysisRhabdomyolysis is due to damage of muscle cells as a result of a variety of factors and can become a unplayful problem (McCance, 20101575). As a result of the damage of muscle cells, its contents (myoglobin, enzymes, potassium and phosphorus) leak into the blood stream. The kidneys secrete myoglobin as myoglobinuria in the pee (Lerma, 2009109).Muscle cell damage can be due to a variety of reasons and amongst others are Trauma, extreme exercise, seizures, compromised blood flow, electrolyte disturbances (such as hypokalemia, hypophosphatemia), drugs, temperature (hyperthermia, burns), inflammation and infections. clinically this disease can vary from mild, with slightly elevated serum levels of myoglobin and creatin kinase (CK) to severe with the necessity for renal replacement therapy. Inci dence of acute kidney failure due to rhabdomyolysis is as high as 5-15% (Greenberg, 2009298-299).Renal insuffiency is due to the ebullient amounts of myoglobin being filtered by the kidney resulting in tubular injury and is generally also associated with hypovolaemia (McPhee, 2009742). Large amounts of myoglobin may clog the nephrons with these being overwhelmed and may pay off casts which will also cause obstruction in the tubules. Hypovolaemia is due to not only a decrease in fluid intake but also due to large amounts of fluid accumulating in the damage muscle tissue (Counts, 2008162-163).Decreased renal blood flow, hypovolaemia and sexually transmitted disease urine all are signs that acute tubular necrosis is likely (Lerma, 2009109).Treatment consists of hydration with high volumes of preferably IV fluids to increase the intravascular fluid volume, thus increase the perfusion of the kidneys and forcing diuresis, reducing the risk of cast formations in the tubules and increas ing the GFR.In severe cases of rhabdomyolis the use of mannitol and bicarbonate to improve urine pH as well as high fluid volumes of up to 12l/24hours have proven beneficial, Dialysis may need to be commenced if urinary output carcass low and with urea and hyperkalemia not responding to conservative treatment (Greenberg, 2009302). Fluid arrangement must be carefully monitored, as there is a risk of pulmonary oedema in the face of acute kidney failure. The mannitol will assist in myoglobin clearance and urine flow and thus assist with the reduction of the nephrotoxicity of the myoglobin. CK levels will drop over a period of a few days provided there is no further injury to the muscle. hypocalcemia is generally not treated in these instances, as the calcium tends to stack up in the injured tissue (Lerma, 2009112).7. ConclusionMany external factors and diseases with origins elsewhere in the body, easily affect the kidney in its function. The above five diseases face just a small p ercentage of the many diseases and dysfunctions which affect the kidney in a multitude of ways and gives us an insight of just how important an organ it is.