Infection With the Human Immunodeficiency Virus133

8/3/2019 Infection With the Human Immunodeficiency Virus133

1/14

1.0 Introduction

1.1. Natural History of HIV infection..

Infection with the Human Immunodeficiency Virus type 1 (HIV-1) and type 2 (HIV-2) is

the primary cause of the Acquired Immunodeficiency Syndromes (AIDS), with HIV-1

accounting for the majority of cases worldwide (1-4). The course of an infection withHIV may be divided into four distinct stages. The first phase is the incubation period,

which is asymptomatic and may last 2-4 weeks. This is followed by the acute phase of

infection lasting an average of 28 days characterized by high viral replication and high

viral load, which may be accompanied by symptoms including lymphadenopathy,pharyngitis, skin rashes, myalgia and malaise(5). After the acute infection, there is a

reduction in plasma viral load probably due to the production of Anti HIV specific

antibodies and T-cells leading to the latency phase that lasts for several years (6;7).During this period there is gradual destruction of the immune system especially as a

result of HIV infecting and destroying CD4+ cells including the T-helper cells. When the

CD4+ cells follow below a critical number, immunity is greatly compromised leading toa wide array of infections and cancers characteristic of the last stage - AIDS. Although

there are reports of survival for up to 25 years after seroconversion, the median survival

is about 12 years but varies considerably between individuals and may be influencedamong other things by race, geographical reasons, sex, virus type and age at

seroconversion(8;9).

1.2 HIV and Organ Function

A wide range of organ malfunction can be attributed to HIV infection, opportunisticinfections and drug toxicities or a combination. Cases of multiple organ failure have also

been reported even in the acute phase of HIV infection (10-12). The introduction of

highly active antiretroviral therapy (HAART) has greatly improved the life expectancyof people living with HIV/AIDS (13;14). HAART however can cause serious metabolic

disturbances such as insulin resistance, disturbances in lipid metabolism and glucose

homeostasis. The metabolic disturbances result into clinical conditions e.g. metabolicsyndrome, hyperlipidemia, lipodystrophy, cardiovascular disease and nephropathies

further complicating the life of an HIV infected individual (15-19).2.0 Renal Function.

The kidney regulates water, electrolyte and acid-base balance and excretes drugs, toxins

as well as products of protein and nucleic acid metabolism e.g. urea, creatinine, uric acid,

sulphate and phosphate. The kidney also produces the hormones erythropoietin, Calcitriol(1,25 Dihydroxycholecalciferol), the active form of vitamin D and the enzyme

Rennin(20). The nephron, a tube with one end closed and the other open, (fig 1) is the

primary functional unit of the kidney and consists of the Glomerulus, the Bowmans

capsule, proximal tubule, the loop of henle and the collecting duct.

The closed end of the tube is pushed in to form a double walled chamber called theBowmans capsule. The Bowmans capsule houses a network of capillaries called the

glomerulus. Blood enterers the glomerulus trough the afferent arteriole (A in figure 1)

under pressure forcing water, small molecules and ions to filter through into theBowmans capsule as the nephric filtrate, blood then leaves through the efferent arteriole


2/14

(E in figure 1). The nephric filtrate collects with in the Bowmans capsule and flows into

the proximal tubes where glucose, amino acids, uric acid and inorganic salts are

reabsorbed by active transport while water follows by osmosis. The active transport ofsodium in the proximal tubules is controlled by angiotensin II while the active transport

of phosphate (PO43-) is controlled by the parathyroid hormone.

Figure 1:The nephron with minor modifications from (21).

A

E

Although only approximately 20% of the nephritic filtrate reaches the loop of henle,

reabsorption from and secretion into the filtrate continues through the distal tubules andthe collecting ducts. The final reabsorption of sodium in the distal tubules is regulated

chiefly by aldosterone and determines the final sodium and water balance and hence the blood pressure. Sodium reabsorption is associated with hydrogen excretion and

reabsorption of chloride and bicarbonate so as to maintain electrostatic equilibrium. Theantidiuretic hormone/ arginine vasopressin (ADH/AVP) produced by the posterior

pituitary controls the reabsorption of water in the distal tubules and the collecting ducts.

ADH is produced in response to increased osmotic pressure as occurs in dehydration andinhibited by reduced osmotic pressure as occurs after drinking large amounts of water.

ADH binds V2 receptors present on cells of the distal tubules leading to increase water

permeability due to insertion of aquaporin-2 channels. If the body needs more water,ADH is produced by the posterior pituitary leading to increased water reabsorption. The

opposite is observed if blood is diluted. The rest of the filtrate is passed out as urine. The

kidney therefore makes urine through three major processes i.e. filtering small moleculesfrom blood, reclaiming/reabsorbing useful materials in the right amounts and excretingexcess water, waste molecules and ions as urine.(20-23).

3.0 Renal Dysfunction.


3/14


4/14

and Fanconi syndrome are some of the other pathologies seen in HIV infected individuals

that may not directly be attributed to HIV infection (45-51).

On the other hand, some renal diseases e.g. HIV associated nephropathy, HIV immune

complex disease are directly attributed to HIV infection(52-56)

4.0. Assessment of Renal Function

Assessment of the state of renal function may be required for several reasons includingestablishment of renal impairment/damage, monitoring of disease progression and

establishment of baseline measurements prior to starting administration of certain drugs

e.g. Antiretroviral therapy.

Generally speaking the prime function of the kidney is the regulation/maintenance of

extracellular fluid composition and volume. It accomplishes these functions through

glomerular filtration and tubular activity. It is the loss of this function that is commonly

referred to as renal failure, which may be acute, characterized by rapid decline in renalfunction that returns to normal within three months or Chronic (CKD) that persists for

more than 3 months(57).

The excretion of soluble waste products such as Urea and Creatinine, foreign materials

e.g. drugs and the maintenance extracellular fluid volume and composition through

electrolyte, water, acid / base balance are accomplished through glomerular and tubularfunction. By determining how well the kidney performs each of these functions, the state

of kidney function can be established. Since no single test can assess overall renal

function, the choice of test to perform or analytes to measure will depend on the reasonfor assessing renal activity and may include the following.

4.1 Urinalysis.

Physical, chemical and microscopic examination of urine can help identify substances

associated with metabolic and/or kidney disorders. Such substances include: -

4.1.1 Proteins greater than >20,000 Daltons are normally not filtered at the glomerulus.

Low molecular weight proteins are filtered but reabsorbed. The presence of proteins in

excess of 30mg/day is therefore a result of glomerular damage or failure of the tubules toadequately reabsorb normally filtered proteins and is the earliest marker of kidney

damage (58-61).

4.1.2 Urinary Specific Gravity (USG) can be used to test the concentrating power ofurine in states of relative dehydration. Normal USG is between 1.003 and 1.030. Lower

values are associated with diuretic use, diabetes insipidus, adrenal insufficiency,

aldosteronism and impaired renal function while higher values are associated withglycosuria, and the syndrome of inappropriate antidiuretic hormone(58;62).

4.1.3 Urinary PH can be affected by several factors including diet with proteins and

acidic fruits causing acid urine while high citrate diets cause alkaline urine(63-65).

Usually urine is acid but the PH can be anywhere between 4.5 and 8. The kidney


5/14

normally acidifies urine by balancing the secretion of H+ and the reabsorption of

biocarbonate. The failure to acidify urine results in accumulation acid in the body a

condition known as Renal Tubular Acidosis (RTA)(66;67). The acid load test is used todiagnose RTA due to diminished H+. It involves administration of ammonium chloride

and measuring urinary PH in urine specimens over 8hours (20;68;69). The determination

of urinary PH is also used in the diagnosis and management of urinary tract infectionsand calculi.

4.1.4 Glucose is completely reabsorbed in the renal tubules and does not appear in urine

unless the blood glucose levels exceed the renal threshold. The presence of glucose inurine is termed as glycosuria. Renal glycosuria is an abnormality in which glucose is

excreted in urine despite normal blood levels due tubular dysfunction. Disturbances in

glucose metabolism as occurs in diabetes mellitus, Cushings syndrome, liver and

pancreatic disease or conditions that cause reduced tubular reabsorption e.g. Fanconissyndrome lead to glycosuria(20).

Several other substances including blood, ketones, nitrites, leukocyte esterase, bilirubin

and urobilinogen may be chemically tested for in urine to aid diagnosis and/or monitoringof various metabolic conditions and Urinary Tract Infection.

The microscopic examination of urine for casts, cells, crystals, and bacteria is performed

to further aid diagnosis of urological, metabolic and/or UTI conditions.

4.2 Biochemical Markers of Renal Function.

Measuring endogenous substances in blood such as creatinine (Cr) formed from the

metabolism of creatine in skeletal muscle and urea a waste product of protein

metabolism that are primarily excreted by the kidneys has been traditionally used toevaluate renal function (70).

4.2.1 Serum creatinine concentration.

The concentration of creatinine in plasma of a health individual is fairly constant. Since

excretion is mainly renal, increased serum creatinine levels therefore may indicate

decreased excretion by the kidney i.e. renal failure. Although serum creatinine

concentrations are generally considered a better maker of renal function, creatinine levelsare also influenced by body mass, age, gender, race, intake and metabolism (71;72).

Creatinine is freely filtered by the glomerulus and under normal urinary flow shows

minimal or no reabsorption. It is however secreted by the tubules and an increase inserum creatinine leads to increased tubular secretion and hence over estimation of GFR.

Because of this serum creatinine levels may not raise until the glomerular filtration rate

(GFR) has moderately reduced making it an insensitive marker of small decreases inGFR characteristic of initial stages of CKD due to the so-called creatinine blind GFR area

(40-70ml/min/1.73m2)(71;73;74).


6/14

The reaction between picric acid and creatinine in an alkaline medium i.e. the Jaff

reaction is the most widely used method for the quantitative determination of creatinine

in body fluids(75). The reaction is not specific as many other substances present inserum/plasma including glucose, ketones, pyruvate as well as creatinine homologs and

derivatives interfere with this reaction (76;77). Attempts to improve the specificity of

the Jaff reaction have been made through several approaches including specificadsorption, extraction of interfering substances, dialysis, measurement at different PH

levels and using kinetic measurements(75;78-81). Enzymatic methods for the

determination of creatinine improve specificity and have been shown to give moreaccurate results provided optimum conditions are met. Enzyme combinations and

combinations of enzymes with the Jaff reaction have been used with some protocols

adapted on automated analyzers making current methods more specific, and less

laborious and practical for routine use (82;83).

4.2.2 Serum urea concentration.

Urea is formed in the liver by the reactions of the Krebs urea cycle and is excreted by the

kidneys. Other factors remaining constant, increased serum urea levels can therefore

indicate decreased excretion i.e. renal failure. Compared to creatinine, serum urea is a

less reliable marker of kidney function as serum levels are influenced by many nonekidney factors. High protein diet, increased tissue breakdown, major gastrointestinal

hemorrhage, stress and corticsteroid therapy can lead to increased serum urea. Up to 70%

of the Urea is passively reabsorbed with water depending on the persons state ofhydration with more urea being reabsorbed in states of dehydration and therefore high

levels may be observed in dehydrated patients with normal renal function. Low serum

urea levels may not necessarily denote normal renal function as they may be due lowprotein diet, liver disease, poor tubular reabsorption or pregnancy.

4.2.3Serum electrolytes.Electrolytes help in the assessment of the tubular function of the kidney. The most

commonly used electrolytes are Sodium (Na+), Potassium (K+), Chloride (Cl-) and

Bicarbonate (HCO3-).

4.3 Estimation of Glomerular Filtration rates (GFR)

4.3. Cystatin C as a maker of renal Function.

4.3 Estimation of Glomerular Filtration rates (GFR) using Prediction Formulas.


7/14

Because of the difficulties associated with the use of exogenous substances in the

estimation of GFR and the pitfalls of using serum creatinine, the search for a betterendogenous marker continues. Cystatin C a 13kDa protease inhibitor belonging to the

cystatin superfamily is a promising molecule. Cystatin C is encoded by housekeeping

gene and is produced by all nucleated cells[44] . It is freely filtered at the glomerulus andnot secreted by the tubules. Unlike creatinine it is not affected by gender, age and muscle

mass[45, 46]. Several studies have demonstrated that cystatin c is superior to creatinine

and urea [47-49]. a recent report has however indicated that Cystatin C is inferior tocreatinine based methods and supports the use of the MDRD formula in HIV infected

individuals but suggests validation in larger studies before generalisation[50] . There is

limited data regarding the use of Cystatin C concentration, GFR estimates based on

cystatin C and those based on creatinine in HIV infected individuals.

Reference List

(1) Barre-Sinoussi F, Chermann JC, Rey F, Nugeyre MT, Chamaret S, Gruest J, et al.

Isolation of a T-lymphotropic retrovirus from a patient at risk for acquiredimmune deficiency syndrome (AIDS). Science 1983 May 20;220(4599):868-71.

(2) Broder S, Gallo RC. A pathogenic retrovirus (HTLV-III) linked to AIDS. N Engl

J Med 1984 Nov 15;311(20):1292-7.

(3) Gallo RC, Salahuddin SZ, Popovic M, Shearer GM, Kaplan M, Haynes BF, et al.

Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from

patients with AIDS and at risk for AIDS. Science 1984 May 4;224(4648):500-3.


8/14

(4) Clavel F, Guetard D, Brun-Vezinet F, Chamaret S, Rey MA, Santos-Ferreira MO,

et al. Isolation of a new human retrovirus from West African patients with AIDS.

Science 1986 Jul 18;233(4761):343-6.

(5) Soogoor M, Daar ES. Primary HIV-1 Infection: Diagnosis, Pathogenesis, and

Treatment. Curr Infect Dis Rep 2005 Mar;7(2):147-53.

(6) Van der Paal L, Shafer LA, Todd J, Mayanja BN, Whitworth JA, Grosskurth H.HIV-1 disease progression and mortality before the introduction of highly active

antiretroviral therapy in rural Uganda. AIDS 2007 Nov;21 Suppl 6:S21-S29.

(7) Lutalo T, Gray RH, Wawer M, Sewankambo N, Serwadda D, Laeyendecker O, et

al. Survival of HIV-infected treatment-naive individuals with documented datesof seroconversion in Rakai, Uganda. AIDS 2007 Nov;21 Suppl 6:S15-S19.

(8) Todd J, Glynn JR, Marston M, Lutalo T, Biraro S, Mwita W, et al. Time fromHIV seroconversion to death: a collaborative analysis of eight studies in six low

and middle-income countries before highly active antiretroviral therapy87. AIDS 2007 Nov;21 Suppl 6:S55-S63.

(9) Qu W, Robinson M, Zhang FJ. Factors influencing the natural history of HIV-1

infection. Chin Med J (Engl ) 2008 Dec 20;121(24):2613-21.

(10) Tattevin P, Camus C, Arvieux C, Ruffault A, Michelet C. Multiple organ failureduring primary HIV infection. Clin Infect Dis 2007 Feb 1;44(3):e28-e29.

(11) Pano-Pardo JR, Alcaide ML, Abbo L, Dickinson G. Primary HIV infection with

multisystemic presentation. Int J Infect Dis 2009 Jul;13(4):e177-e180.

(12) Grigoriu BD, Jacobs FM, Mas AE, Prat D, Prevot S, Brivet FG. [Disseminated

tuberculosis with severe multi- organ failure in a patient with AIDS]. Rev Mal

Respir 2008 Sep;25(7):853-6.

(13) Gortmaker SL, Hughes M, Cervia J, Brady M, Johnson GM, Seage GR, III, et al.

Effect of combination therapy including protease inhibitors on mortality amongchildren and adolescents infected with HIV-1. N Engl J Med 2001 Nov

22;345(21):1522-8.

(14) Palella FJ, Jr., Delaney KM, Moorman AC, Loveless MO, Fuhrer J, Satten GA, et

al. Declining morbidity and mortality among patients with advanced human

immunodeficiency virus infection. HIV Outpatient Study Investigators. N Engl JMed 1998 Mar 26;338(13):853-60.

(15) Samaras K. Prevalence and pathogenesis of diabetes mellitus in HIV-1 infection

treated with combined antiretroviral therapy. J Acquir Immune Defic Syndr 2009

Apr 15;50(5):499-505.


9/14

(16) Samaras K. Metabolic consequences and therapeutic options in highly active

antiretroviral therapy in human immunodeficiency virus-1 infection. J Antimicrob

Chemother 2008 Feb;61(2):238-45.

(17) Wand H, Calmy A, Carey DL, Samaras K, Carr A, Law MG, et al. Metabolic

syndrome, cardiovascular disease and type 2 diabetes mellitus after initiation ofantiretroviral therapy in HIV infection. AIDS 2007 Nov 30;21(18):2445-53.

(18) Bradbury RA, Samaras K. Antiretroviral therapy and the human

immunodeficiency virus--improved survival but at what cost? Diabetes Obes

Metab 2008 Jun;10(6):441-50.

(19) Daugas E, Rougier JP, Hill G. HAART-related nephropathies in HIV-infectedpatients. Kidney Int 2005 Feb;67(2):393-403.

(20) Allan Gaw, Robert A Cowan, Denis St.J.OReilly, Micheael J Stewart, JamesShepherd. Investigation Of Renal Function. Clinical Biochemistry. Churchill

Livingstone; 1995.

(21) . 2009. 6-2-2009.

Ref Type: Internet Communication

(22) F.J.Baker, R.E.Silverton. Renal Function Tests. Introduction to Medical

Laboratory Technology. 6 ed. Butterworths; 2009. p. 140-60.

(23) Monica Cheesbrough. Urinary System. Medical Laboratory Manual for TropicalCountries. Second Edition ed. Tropical Health Technology; 2009. p. 104-9.

(24) Siren AL, Ehrenreich H. Erythropoietin--a novel concept for neuroprotection. EurArch Psychiatry Clin Neurosci 2001 Aug;251(4):179-84.

(25) Siren AL, Fratelli M, Brines M, Goemans C, Casagrande S, Lewczuk P, et al.

Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic

stress. Proc Natl Acad Sci U S A 2001 Mar 27;98(7):4044-9.

(26) Ehrenreich H, Aust C, Krampe H, Jahn H, Jacob S, Herrmann M, et al.

Erythropoietin: novel approaches to neuroprotection in human brain disease.Metab Brain Dis 2004 Dec;19(3-4):195-206.

(27) Haroon ZA, Amin K, Jiang X, Arcasoy MO. A novel role for erythropoietin

during fibrin-induced wound-healing response5. Am J Pathol 2003 Sep;163(3):993-1000.

(28) Schuster SJ, Koury ST, Bohrer M, Salceda S, Caro J. Cellular sites of extrarenal

and renal erythropoietin production in anaemic rats. Br J Haematol 1992Jun;81(2):153-9.


10/14

(29) Bosman DR, Winkler AS, Marsden JT, Macdougall IC, Watkins PJ. Anemia with

erythropoietin deficiency occurs early in diabetic nephropathy. Diabetes Care

2001 Mar;24(3):495-9.

(30) Nurko S. Anemia in chronic kidney disease: causes, diagnosis, treatment. Cleve

Clin J Med 2006 Mar;73(3):289-97.

(31) Jones G, Strugnell SA, Deluca HF. Current understanding of the molecularactions of vitamin D. Physiol Rev 1998 Oct;78(4):1193-231.

(32) Underwood JL, DeLuca HF. Vitamin D is not directly necessary for bone growth

and mineralization. Am J Physiol 1984 Jun;246(6 Pt 1):E493-E498.

(33) Micheal L.Bishop, Janet L.Duben-Engelkirt, Edward P.Fody. Clinical Chemistry,

Principles,procedures ,Correlations. Fourth Edition ed. 2000.

(34) Causes of death. USRDS. United States Renal Data System. Am J Kidney Dis

1997 Aug;30(2 Suppl 1):S107-S117.

(35) Izzedine H, Launay-Vacher V, Deray G. Antiviral drug-induced nephrotoxicity

4. Am J Kidney Dis 2005 May;45(5):804-17.

(36) Izzedine H, Launay-Vacher V, Isnard-Bagnis C, Deray G. Drug-inducedFanconi's syndrome

6. Am J Kidney Dis 2003 Feb;41(2):292-309.

(37) Cohen AH, Sun NC, Shapshak P, Imagawa DT. Demonstration of human

immunodeficiency virus in renal epithelium in HIV-associated nephropathy

4. Mod Pathol 1989 Mar;2(2):125-8.

(38) Cohen AH, Nast CC. HIV-associated nephropathy. A unique combinedglomerular, tubular, and interstitial lesion

5. Mod Pathol 1988 Mar;1(2):87-97.

(39) Jones R, Scott C, Nelson M, Levy J. Renal complications in HIV

3. Int J Clin Pract 2007 Jun;61(6):991-8.

(40) Gupta SK, Eustace JA, Winston JA, Boydstun II, Ahuja TS, Rodriguez RA, et al.

Guidelines for the management of chronic kidney disease in HIV-infectedpatients: recommendations of the HIV Medicine Association of the Infectious

Diseases Society of America1. Clin Infect Dis 2005 Jun 1;40(11):1559-85.

(41) Valeri A, Neusy AJ. Acute and chronic renal disease in hospitalized AIDS

patients5. Clin Nephrol 1991 Mar;35(3):110-8.


11/14

(42) Castro-Sansores CJ, Santos-Rivero A, Lara-Perera D, Gonzalez-Martinez P,

Alonso-Salomon G, Gongora-Biachi RA. [Hyperlipidemia and glucose

intolerance in patients with HIV infection receiving antiretroviral therapy]. SaludPublica Mex 2006 May;48(3):193-9.

(43) Barbaro G. Pathogenesis of HIV-associated heart disease. AIDS 2003 Apr;17Suppl 1:S12-S20.

(44) Berns JS, Cohen RM, Stumacher RJ, Rudnick MR. Renal aspects of therapy for

human immunodeficiency virus and associated opportunistic infections

1. J Am Soc Nephrol 1991 Mar;1(9):1061-80.

(45) Cheng JT, Anderson HL, Jr., Markowitz GS, Appel GB, Pogue VA, D'Agati VD.Hepatitis C virus-associated glomerular disease in patients with human

immunodeficiency virus coinfection. J Am Soc Nephrol 1999 Jul;10(7):1566-74.

(46) Szczech LA, Gupta SK, Habash R, Guasch A, Kalayjian R, Appel R, et al. The

clinical epidemiology and course of the spectrum of renal diseases associated withHIV infection. Kidney Int 2004 Sep;66(3):1145-52.

(47) Kimmel PL, Phillips TM, Ferreira-Centeno A, Farkas-Szallasi T, Abraham AA,

Garrett CT. Brief report: idiotypic IgA nephropathy in patients with humanimmunodeficiency virus infection. N Engl J Med 1992 Sep 3;327(10):702-6.

(48) Rollot F, Nazal EM, Chauvelot-Moachon L, Kelaidi C, Daniel N, Saba M, et al.

Tenofovir-related Fanconi syndrome with nephrogenic diabetes insipidus in a

patient with acquired immunodeficiency syndrome: the role of lopinavir-ritonavir-didanosine. Clin Infect Dis 2003 Dec 15;37(12):e174-e176.

(49) Karras A, Lafaurie M, Furco A, Bourgarit A, Droz D, Sereni D, et al. Tenofovir-related nephrotoxicity in human immunodeficiency virus-infected patients: three

cases of renal failure, Fanconi syndrome, and nephrogenic diabetes insipidus. Clin

Infect Dis 2003 Apr 15;36(8):1070-3.

(50) Verhelst D, Monge M, Meynard JL, Fouqueray B, Mougenot B, Girard PM, et al.Fanconi syndrome and renal failure induced by tenofovir: a first case report. Am J

Kidney Dis 2002 Dec;40(6):1331-3.

(51) Izzedine H, Isnard-Bagnis C, Hulot JS, Vittecoq D, Cheng A, Jais CK, et al.

Renal safety of tenofovir in HIV treatment-experienced patients. AIDS 2004 Apr

30;18(7):1074-6.

(52) Marras D, Bruggeman LA, Gao F, Tanji N, Mansukhani MM, Cara A, et al.

Replication and compartmentalization of HIV-1 in kidney epithelium of patientswith HIV-associated nephropathy. Nat Med 2002 May;8(5):522-6.

(53) Leventhal JS, Ross MJ. Pathogenesis of HIV-associated nephropathy. Semin

Nephrol 2008 Nov;28(6):523-34.


12/14

(54) Lu TC, Ross M. HIV-associated nephropathy: a brief review. Mt Sinai J Med

2005 May;72(3):193-9.

(55) Ross MJ, Klotman PE. HIV-associated nephropathy. AIDS 2004 May

21;18(8):1089-99.

(56) Ross MJ, Klotman PE, Winston JA. HIV-associated nephropathy: case study and

review of the literature. AIDS Patient Care STDS 2000 Dec;14(12):637-45.

(57) Levey AS, Coresh J, Balk E, Kausz AT, Levin A, Steffes MW, et al. NationalKidney Foundation practice guidelines for chronic kidney disease: evaluation,

classification, and stratification. Ann Intern Med 2003 Jul 15;139(2):137-47.

(58) Simerville JA, Maxted WC, Pahira JJ. Urinalysis: a comprehensive review

1. Am Fam Physician 2005 Mar 15;71(6):1153-62.

(59) Keane WF, Eknoyan G. Proteinuria, albuminuria, risk, assessment, detection,

elimination (PARADE): a position paper of the National Kidney Foundation. AmJ Kidney Dis 1999 May;33(5):1004-10.

(60) Keane WF. Proteinuria: its clinical importance and role in progressive renaldisease. Am J Kidney Dis 2000 Apr;35(4 Suppl 1):S97-105.

(61) Standards of medical care for patients with diabetes mellitus. Diabetes Care 2002

Jan;25(1):213-29.

(62) Kavouras SA. Assessing hydration status. Curr Opin Clin Nutr Metab Care 2002

Sep;5(5):519-24.

(63) Sheets C, Lyman JL. Urinalysis. Emerg Med Clin North Am 1986 May;4(2):263-

80.

(64) Kiel DP, Moskowitz MA. The urinalysis: a critical appraisal. Med Clin North Am

1987 Jul;71(4):607-24.

(65) Benejam R, Narayana AS. Urinalysis: the physician's responsibility. Am FamPhysician 1985 Jan;31(1):103-11.

(66) Laing CM, Unwin RJ. Renal tubular acidosis. J Nephrol 2006 Mar;19 Suppl

9:S46-S52.

(67) Laing CM, Toye AM, Capasso G, Unwin RJ. Renal tubular acidosis:

developments in our understanding of the molecular basis. Int J Biochem Cell

Biol 2005 Jun;37(6):1151-61.

(68) Laing CM, Toye AM, Capasso G, Unwin RJ. Renal tubular acidosis:

developments in our understanding of the molecular basis4. Int J Biochem Cell Biol 2005 Jun;37(6):1151-61.


13/14

(69) Laing CM, Unwin RJ. Renal tubular acidosis

2. J Nephrol 2006 Mar;19 Suppl 9:S46-S52.

(70) Perrone RD, Madias NE, Levey AS. Serum creatinine as an index of renal

function: new insights into old concepts

18. Clin Chem 1992 Oct;38(10):1933-53.

(71) Swedko PJ, Clark HD, Paramsothy K, Akbari A. Serum creatinine is aninadequate screening test for renal failure in elderly patients. Arch Intern Med

2003 Feb 10;163(3):356-60.

(72) Duncan L, Heathcote J, Djurdjev O, Levin A. Screening for renal disease using

serum creatinine: who are we missing? Nephrol Dial Transplant 2001May;16(5):1042-6.

(73) Dourado R, Queiroz e Melo, Abecasis J, Ferreira A, Barata JD, Rebocho MJ, etal. Serum creatinine values underestimate surgical risk. Rev Port Cardiol 2009

Mar;28(3):269-78.

(74) Perrone RD, Madias NE, Levey AS. Serum creatinine as an index of renal

function: new insights into old concepts. Clin Chem 1992 Oct;38(10):1933-53.

(75) SLOT C. Plasma creatinine determination. A new and specific Jaffe reaction

method4. Scand J Clin Lab Invest 1965;17(4):381-7.

(76) Blass KG, Thibert RJ, Lam LK. A study of the mechanism of the Jaffe reaction. Z

Klin Chem Klin Biochem 1974 Jul;12(7):336-43.

(77) Narayanan S, Appleton HD. Creatinine: a review. Clin Chem 1980

Jul;26(8):1119-26.

(78) Hare RS. Endogenous creatinine in serum and urine. Proc Soc Exp Biol Med

1950 May;74(1):148-51.

(79) Taussky HH. A procedure increasing the specificity of the Jaffe reaction for the

determination of creatine and creatinine in urine and plasma. Clin Chim Acta1956 May;1(3):210-24.

(80) CHASSON AL, GRADY HJ, STANLEY MA. Determination of creatinine by

means of automatic chemical analysis. Tech Bull Regist Med Technol 1960Dec;30:207-12.

(81) Heinegard D, Tiderstrom G. Determination of serum creatinine by a direct

colorimetric method. Clin Chim Acta 1973 Feb 12;43(3):305-10.

(82) Masson P, Ohlsson P. Improved precision of the enzymic-Jaffe method fordetermination of creatinine. Clin Chem 1981 Jun;27(6):1139.


14/14

(83) Masson P, Ohlsson P, Bjorkhem I. Combined enzymic-Jaffe method for

determination of creatinine in serum. Clin Chem 1981 Jan;27(1):18-21.

0772-446,747

Infection With the Human Immunodeficiency Virus133

Documents

Transcript of Infection With the Human Immunodeficiency Virus133