History

Fact Explanation
Duration of the disease [4] Kidney disease can be either acute or chronic kidney disease. Chronic kidney disease is a condition with kidney damage, manifested by abnormal albumin excretion or decreased kidney function,characterized by irreversible loss of renal function [3] lasting for more than three months. [4] It is associated with increased incidence of cardiovascular disease, hyperlipidemia, anemia and metabolic bone disease. [4] National Kidney Foundation has developed criteria, to identify the five stages of the disease according to the estamated GFR values. [4] Once there is a significant impairment of renal function, the deterioration occurs irrespective of the underlying kidney disorder. Hypertension and proteinuria are two main factors in the progression of CKD. [5]
Features of uremia [8] : impaired consciousness, pruritus, darkening of the skin, nausea, vomiting, hiccups Impaired excretion of waste products is associated with elevation of blood urea [9] giving rise to various adverse symptoms and signs.
Fractures and bone pain [4] There can be abnormal bone and mineral metabolism, extra-skeletal calcification in patients with CKD. [4] kidney is important for the phosphate excretion and 1-α-hydroxylation of vitamin D. In CKD, the level of phosphate is increaed and the level of vitamin D is reduced. There is a spectrum of manifestations i these patiebts which is renal osteodystrophy. [4] Secondary hyperparathyroidism develops, lesding to frequent fractures and bone pain.
Shortness of breath on exertion, fatigue and lethargy [3] Anamia is a frequent finding in chronic kidney disease patients, that increases the risk of poor outcome. Various factors are contributing to the developmant of anaemia in these patients. Iron and erythropoietin deficiencies and hyporesponsiveness to the actions of erythropoietin (requirement for high doses of erythropoietin in order to raise blood Hb level in the absence of iron deficiency), [1,4] reduced bone marrow production of the erythroblasts, increased red cell destruction and poor dietary intake are some of the mechanisms involved in the pathogenesis of anaemia. Increased levels of inflammatory cytokines increase the level of hepcidin, It impairs the intestinal iron absorption and iron transport from the reticuloendothelial system to bone marrow. [1] Drugs such as ACE inhibitors and angiotensin receptor antagonists may also contributes to the anaemia by transient lowering of the level of haemoglobin. [1]
Recurrent infections [3] Chronic kidney disease patients are vulnerable to frequent infections due to the impaired immune function and vascular compromise. [3] Immune deficiency is due to the impairment in structure and function of the innate immune system,and adaptive immunity including T and B lymphocytes. [8]
History of myocardial infarction, angina and stroke [3] Cardiovascular diseases are the leading causes of death in patients with CKD, particularly in patients with diabetes. [1] Low Hb concentration is an recognized risk factor for the development of heart failure, and cardiovascular diseases. Uremia, inflammation, obesity, erythropoiesis-stimulating agents and iron therapy are the other contributory factors for the increase cardiovascula disease risk. [2] Coronary artery calcification is also more frequent in these patients ddue to the abnormal mineral metabolism with high phosphorus, calcium-phosphorus product, and PTH. [2]
History of diabetes mellitus [1] Diabetes mellitus is a main risk factor for the development of CKD. Diabetei nephropathy is a recognised complication of diabetes mellitus, in both type 1 and 2. [1,3]
Dyslipidaemia [5] This is an independent risk factor for both cardiovascular disease and for progressive chronic renal failure. [5]
Features of thromboembolism[6] :severe leg pain, dificulty in breathing Chronic kidney disease patients are vulnerable for venous thromboembolism due to various factors such as activation of procoagulation, enhanced platelet activation and aggregation, decreased anticoagulation in the body, and decreased activity of fibrinolytic system. [6]
Abnormalities of the urinary tract [5] Congenital renal hypodysplasia with or without urinary tract abnormalities is the cause of chronic kidney disease in more than 60% of children. [5] Reflux nephropathy is associated with vesicoureteric reflux disease. [7]
History of features suggestive of glomerulonephritis [7] eg: recurrent episodes of haematuria IgA nephropathy and nephritic syndrome can occasionally lead to CKD. Focal segmental glomerulosclerosis responsible for the majority of CKD due to the glomerulonephritis. [7]
Features of psychological problems : Fatigue, changes in appetite and sleep pattern CKD is a chronic medical condition associated with various psychological comorbidities. Biological changes and complications associated with chronic medical disorders may precipitate these problems.[10] Chronic disaese patients are vulnerable to depression, anxiety, substance abuse and suicide. It might also adversly affect the adherence to medication and recommended treatment strategies. [11]
References
  1. MEHDI U, TOTO RD. Anemia, Diabetes, and Chronic Kidney Disease Diabetes Care [online] 2009 Jul, 32(7):1320-1326 [viewed 08 September 2014] Available from: doi:10.2337/dc08-077
  2. MITSNEFES MM. Cardiovascular Disease in Children with Chronic Kidney Disease J Am Soc Nephrol [online] 2012 Apr, 23(4):578-585 [viewed 09 September 2014] Available from: doi:10.1681/ASN.2011111115
  3. SHIRAISHI FG, STRINGUETTA BELIK F, OLIVEIRA E SILVA VR, MARTIN LC, HUEB JC, GONçALVES RD, CARAMORI JC, BARRETI P, FRANCO RJ. Inflammation, Diabetes, and Chronic Kidney Disease: Role of Aerobic Capacity Exp Diabetes Res [online] 2012:750286 [viewed 09 September 2014] Available from: doi:10.1155/2012/750286
  4. THOMAS R, KANSO A, SEDOR JR. Chronic Kidney Disease and Its Complications Prim Care [online] 2008 Jun, 35(2):329-vii [viewed 09 September 2014] Available from: doi:10.1016/j.pop.2008.01.008
  5. WüHL E, SCHAEFER F. Therapeutic strategies to slow chronic kidney disease progression Pediatr Nephrol [online] 2008 May, 23(5):705-716 [viewed 09 September 2014] Available from: doi:10.1007/s00467-008-0789-y
  6. WATTANAKIT K, CUSHMAN M. Chronic kidney disease and venous thromboembolism: epidemiology and mechanisms Curr Opin Pulm Med [online] 2009 Sep, 15(5):408-412 [viewed 09 September 2014] Available from: doi:10.1097/MCP.0b013e32832ee371
  7. WARADY BA, CHADHA V. Chronic kidney disease in children: the global perspective Pediatr Nephrol [online] 2007 Dec, 22(12):1999-2009 [viewed 09 September 2014] Available from: doi:10.1007/s00467-006-0410-1
  8. VAZIRI ND, PAHL MV, CRUM A, NORRIS K. EFFECT OF UREMIA ON STRUCTURE AND FUNCTION OF IMMUNE SYSTEM J Ren Nutr [online] 2012 Jan, 22(1):149-156 [viewed 09 September 2014] Available from: doi:10.1053/j.jrn.2011.10.020
  9. MERIKAS G, MARKETOS S, KONSTANTOPOULOS E. Uremic pericardial tamponade. Can Med Assoc J [online] 1966 Jul 16, 95(3):119-123 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1936728
  10. SIMON GE. Treating depression in patients with chronic disease West J Med [online] 2001 Nov, 175(5):292-293 [viewed 13 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071593
  11. J. KATON W. Epidemiology and treatment of depression in patients with chronic medical illness Dialogues Clin Neurosci [online] 2011 Mar, 13(1):7-23 [viewed 13 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181964

Examination

Fact Explanation
Pallor [1] Anaemia is a common finding in chroniC kidney disease patients. [1]
Peripheral oedema There is increased sodium and water retention in these patients. [1] They will also have low serum protein contributing to the development of oedema.
Features of nutritional deficiency [1]:Koilonoychia, glossitis, angular stomatitis Dietary deficiency, low intestinal absorption, and gastrointestinal bleeding may cause iron-deficiency anemia. [1] Vitamin B12 and folic acid deficiency is also found due to the reduced dietary intake.
Features of uremia [4] :altered level of consciousness, scratch marks, pigmentation of the body Impaired excretion of waste products is associated with elevation of blood urea [5] giving rise to various adverse symptoms and signs.
Ballotable masses Polycystic kidney disease is a inherited condition in an autosomal dominant fashion [6] and is a cause of CKD.
Abdominal surgical scars Due to renal replacement with kidney transplant. [2]
High blood pressure [5] This can be an associated comorbidity or a side effect of the medications such as erythropoietin stimulating agents. [1]
Features of heart failure [1] : Dyspnea on exertion, elevated jugular venous pressure, shifted cardiac apex, bibasal fine crepitations Heart failure is a common complication among the patients with CKD. Anemia may also aggravate tissue hypoxia, and then the heart failure. [1]
Features of glomerulonephritis [3] : Recurrent episodes of reduced urine output, hypertension and periorbital oedema CKD may be due to the glomerulonephritis. [3]
Features of dabetes mellitus [1] : peripheral neuropathy, joint deformity, ulcers, amputation stumps Diabetes mellitus is a leading cause of chronic kidney disease. [1]
Features of pericardial tamponade [5]: pericardial friction rub This is usually due to uremia causing increased vascular permeability and serositis that result in pericarditis, it is a haemorrhagic pericarditis due to the rupture of the vessles in the area of pericarditis. [5]
Low mood, anxiety Depression and anxiety are commonly associated with chronic disaeses. [7] It may be related to biological changes and complications of the disease. [8]
References
  1. MEHDI U, TOTO RD. Anemia, Diabetes, and Chronic Kidney Disease Diabetes Care [online] 2009 Jul, 32(7):1320-1326 [viewed 08 September 2014] Available from: doi:10.2337/dc08-077
  2. WEBB N, JOHNSON R, POSTLETHWAITE R. Renal transplantation Arch Dis Child [online] 2003 Oct, 88(10):844-847 [viewed 09 September 2014] Available from: doi:10.1136/adc.88.10.844
  3. WARADY BA, CHADHA V. Chronic kidney disease in children: the global perspective Pediatr Nephrol [online] 2007 Dec, 22(12):1999-2009 [viewed 09 September 2014] Available from: doi:10.1007/s00467-006-0410-1
  4. VAZIRI ND, PAHL MV, CRUM A, NORRIS K. EFFECT OF UREMIA ON STRUCTURE AND FUNCTION OF IMMUNE SYSTEM J Ren Nutr [online] 2012 Jan, 22(1):149-156 [viewed 09 September 2014] Available from: doi:10.1053/j.jrn.2011.10.020
  5. MERIKAS G, MARKETOS S, KONSTANTOPOULOS E. Uremic pericardial tamponade. Can Med Assoc J [online] 1966 Jul 16, 95(3):119-123 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1936728
  6. ELLES RG, HODGKINSON KA, MALLICK NP, O'DONOGHUE DJ, READ AP, RIMMER S, WATTERS EA, HARRIS R. Diagnosis of adult polycystic kidney disease by genetic markers and ultrasonographic imaging in a voluntary family register. J Med Genet [online] 1994 Feb, 31(2):115-120 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1049671
  7. J. KATON W. Epidemiology and treatment of depression in patients with chronic medical illness Dialogues Clin Neurosci [online] 2011 Mar, 13(1):7-23 [viewed 13 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181964
  8. SIMON GE. Treating depression in patients with chronic disease West J Med [online] 2001 Nov, 175(5):292-293 [viewed 13 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071593

Differential Diagnoses

Fact Explanation
Acute Kidney Injury Acute kidney injury (AKI) is a common and serious problem associated with high rate of mortality. Acute Physiology and Chronic Health Evaluation (APACHE) II and III, Sequential Organ Failure Assessment (SOFA) and Risk, Injury, Failure, Loss, and End-stage (RIFLE) classification are the methods used to evaluate the AKI. [1] AKI differes from the CKD, as this is of sudden onset of renal dysfunction usually over hours to days. Oliguria/ anuria of may be the presentation. [2] Causes may be divided into prerenal, renal, and postrenal causes. [3] Prerenal causes may be corrected by volume resuscitation that may correct hypovolemia. [3] Plasma creatinine, blood urea nitrogen, urine electrolytes, urinalysis, and ultrasound, may be helpful to make a diagnosis. [3] Fluid management, and fluid balance is critical in the management of these patients. [2]
Aetiology: Chronic Glomerulonephritis [6] Glomerulonephritis is associated with inflammation of the glomeruli, trhat can progress into irreversible and progressive glomerular and tubulointerstitial fibrosis, leading to CKD.Patient may have a past history of recurrent haematuria, froth in the urine due to proteinuria, oliguria, peripheral oedema etc. Diagnosis of the exact aetiology may need examination under electron microscopy and immunofluriscence. [6]
Aetiology : Diabetic Nephropathy [5] Diabetic nephropathy is associated with persistent albuminuria (>300 mg/d or >200 μg/min), progressive decline in the glomerular filtration rate (GFR) and elevated arterial blood pressure in a diabetic patient. Mesangial expansion, thickening of the glomerular basement membrane (GBM) and glomerular sclerosis are the pathological changes in this condition. [4] Microalbuminuria is the initial step in the pathogenesis of the nephropathy. [5]
Aetiology : Alport syndrome This is a type of a nephritis associated with progressive deterioration of the glomerular basement membrane and loss of renal function. It is also associated with progressive hearing loss. [10] Renal failure in usually occurs in the 4th or 5th decade. [10] They can have common non-specific clinical symptoms such as progressive proteinuria and sustained hypoalbuminemia. [11] Diagnosis may require renal biopsy and histological evaluation. [11]
Aetiology : Goodpasture syndrome [9] Goodpasture syndrome is associated with kidney disease consistent with glomerulonephritis [9] and lung disease associated with pulmonary haemorrhage. Pleuritic chest pain, haemoptysis, increasing dyspnea on exertion, haematuria are the possible clinical manifestations and they may have red cell casts in the urinalysis, recurrent pulmonary infiltrates and haemorrhagic pneumonitis. [12] Plasma exchange, cyclophosphamide and prednisilone are used for the treatment. [12]
Aetiology : Rapidly progressive glomerulonephritis [7] This is a condition that is associated with rapid decline of renal function [7] over a few days to 3 months. Generalised body swelling may be accompanied by oliguria. [7] There are other features of glomerulonephritis associated with rapid loss of renal function. [8] It is seen in amyloidosis, henoch schonlein purpura and in any form of a renal vasculitis. [8]
References
  1. SHARIFIPOUR F, HAMI M, NAGHIBI M, ZERAATI A, ARIAN S, AZARIAN AA. RIFLE criteria for acute kidney injury in the intensive care units J Res Med Sci [online] 2013 May, 18(5):435-437 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810581
  2. GRAMS ME, ESTRELLA MM, CORESH J, BROWER RG, LIU KD, FOR THE NATIONAL HEART, LUNG, AND BLOOD INSTITUTE ACUTE RESPIRATORY DISTRESS SYNDROME NETWORK. Fluid Balance, Diuretic Use, and Mortality in Acute Kidney Injury Clin J Am Soc Nephrol [online] 2011 May, 6(5):966-973 [viewed 09 September 2014] Available from: doi:10.2215/CJN.08781010
  3. HIMMELFARB J, JOANNIDIS M, MOLITORIS B, SCHIETZ M, OKUSA MD, WARNOCK D, LAGHI F, GOLDSTEIN SL, PRIELIPP R, PARIKH CR, PANNU N, LOBO SM, SHAH S, D'INTINI V, KELLUM JA. Evaluation and Initial Management of Acute Kidney Injury Clin J Am Soc Nephrol [online] 2008 Jul, 3(4):962-967 [viewed 09 September 2014] Available from: doi:10.2215/CJN.04971107
  4. MAUER SM, STEFFES MW, ELLIS EN, SUTHERLAND DE, BROWN DM, GOETZ FC. Structural-functional relationships in diabetic nephropathy. J Clin Invest [online] 1984 Oct, 74(4):1143-1155 [viewed 09 September 2014] Available from: doi:10.1172/JCI111523
  5. BARUTTA F, CORBELLI A, MASTROCOLA R, GAMBINO R, DI MARZO V, PINACH S, RASTALDI MP, PERIN PC, GRUDEN G. Cannabinoid Receptor 1 Blockade Ameliorates Albuminuria in Experimental Diabetic Nephropathy Diabetes [online] 2010 Apr, 59(4):1046-1054 [viewed 09 September 2014] Available from: doi:10.2337/db09-1336
  6. HARRISON DJ, THOMSON D, MACDONALD MK. Membranous glomerulonephritis. J Clin Pathol [online] 1986 Feb, 39(2):167-171 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC499671
  7. ANUPAMA YJ, VANKALAKUNTI M. Rapidly progressive glomerulonephritis in a patient with renal amyloidosis: Case report and review of the literature Indian J Nephrol [online] 2012, 22(5):377-380 [viewed 11 September 2014] Available from: doi:10.4103/0971-4065.103931
  8. SOZERI B, MIR S, ERTAN P, KARA OD, SEN S. Rapidly progressive glomerulonephritis in a child with Henoch-Sch?nlein Vasculitis and familial Mediterranean fever Pediatr Rheumatol Online J [online] :8 [viewed 11 September 2014] Available from: doi:10.1186/1546-0096-7-8
  9. HASSTEDT SJ, ATKIN CL, SAN JUAN AC JR. Genetic heterogeneity among kindreds with Alport syndrome. Am J Hum Genet [online] 1986 Jun, 38(6):940-953 [viewed 11 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1684840
  10. BARKER DF, PRUCHNO CJ, JIANG X, ATKIN CL, STONE EM, DENISON JC, FAIN PR, GREGORY MC. A mutation causing Alport syndrome with tardive hearing loss is common in the western United States. Am J Hum Genet [online] 1996 Jun, 58(6):1157-1165 [viewed 12 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1915056
  11. YAO XIAO-DAN, CHEN XIN, HUANG GAO-YUAN, YU YAN-TING, XU SHU-TIAN, HU YANG-LIN, WANG QING-WEN, CHEN HUI-PING, ZENG CAI-HONG, JI DA-XI, HU WEI-XIN, TANG ZHENG, LIU ZHI-HONG. Challenge in pathologic diagnosis of Alport syndrome: evidence from correction of previous misdiagnosis. Array [online] 2012 December [viewed 12 September 2014] Available from: doi:10.1186/1750-1172-7-100
  12. ROSSEN RD, DUFFY J, MCCREDIE KB, REISBERG MA, SHARP JT, HERSH EM, EKNOYAN G, SUKI WN. Treatment of Goodpasture syndrome with cyclophosphamide, prednisone and plasma exchange transfusions. Clin Exp Immunol [online] 1976 Apr, 24(1):218-222 [viewed 12 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1538509

Investigations - for Diagnosis

Fact Explanation
Albuminuria [1] Both macro and micro albuminuria increases the risk ofdisease progression [12] and mortality among the patients with CKD. [1] Microalbuminuria (urine albumin excretion 30 mg/ 24hr) [2] increases the cardiovascular disease risk.
Estimated Glomerular filtration rate (GFR) [1] This is calculated with the serum creatinine concentration, using either the Cockcroft-Gault or the Modification of Diet in Renal Disease (MDRD) Study estimating equations. [2] The level of estimated GFR <60 ml/min per 1.73 m2 is associated with incraesed mortality in CKD patients. [3] MDRD equation overestimates renal function when assesing the GFR. According to the eGFR value, the 5 stages of the CKD are, Stage 1: normal eGFR ≥ 90 mL/min per 1.73 m2 and persistent albuminuria, stage 2: eGFR between 60 to 89 mL/min per 1.73 m2, stage 3: eGFR between 30 to 59 mL/min per 1.73 m2, stage 4: eGFR between 15 to 29 mL/min per 1.73 m2, and stage 5: eGFR of < 15 mL/min per 1.73 m2. [2]
Creatinine clearance [2] Calculated from urine creatinine concentration within a 24 hour period, butserum creatinine have a less practical value when compared to eGFR. [2]
Blood urea (BUN) [12] Impaired renal functions are associated with increased accumulation of waste products in the blood such as urea. BUN, >15 mmol/L is considered as abnormal. [12]
Serum electrolytes [12] Hyperkalemia [12] is the most common clinically significant electrolyte abnormality in these patients. [11] Hyponatremia, hypocalcemia, and hypermagnesemia may develop during the dialysis therapy.
Imaging modalities : ultrasound scan, x-ray [4] USS is useful to screen for hydronephrosis, shrunken small kidneys in advanced kidney failure, normal sized kidneys in diabetic nephropathy and vascular abnormalities. [5] Autosomal dominant adult polycystic kidney diseasecan be diagnosed by ultrasonographic scanning (USS) or by using DNA markers linked to the PKD1 locus. [10] Doppler-derived renal resistive index has been used to estimate the risk of progression in CKD. It is also used in transplant reciepients to evaluate the prognosis. [5] X-ray can be used to evaluate the ureteric stones, dialatation of the pelvicalyceal system and bone disease in advanced chronic kidney disease. [4]
CT/MRI and radionuclide imaging Magnetic resonance imaging (MRI) and Computed tomography (CT)are used for the evaluation of renal abnormalities. [7] Cysts, malignancies, polycystic kidney disease can be detected using these methods. Usually MRI is performed only after detection of the renal lesion by ultrasound or CT. [7] Gadolinium enhancement is used to measure the kidney volume. [8] It is an important marker to determine disease progression and overall prognosis. [9]
Renal biopsy [3] Diagnosis of vasculitis and rapidly progressive glomerulonephritis may need by renal biopsy. [3]
Serum Cystatin C levels Serum cystatin C can be used as a marker of renal failure and is able to replace the serum creatinine (Scr) in glomerular filtration rate (GFR) estimation. GFR estimate usind serum cystatin levels is accurate as Scr used estimate and is not ralated to the muscle mass. [6]
References
  1. GROOP PH, THOMAS MC, MORAN JL, WADèN J, THORN LM, MäKINEN VP, ROSENGåRD-BäRLUND M, SARAHEIMO M, HIETALA K, HEIKKILä O, FORSBLOM C. The Presence and Severity of Chronic Kidney Disease Predicts All-Cause Mortality in Type 1 Diabetes Diabetes [online] 2009 Jul, 58(7):1651-1658 [viewed 09 September 2014] Available from: doi:10.2337/db08-1543
  2. THOMAS R, KANSO A, SEDOR JR. Chronic Kidney Disease and Its Complications Prim Care [online] 2008 Jun, 35(2):329-vii [viewed 09 September 2014] Available from: doi:10.1016/j.pop.2008.01.008
  3. HIGGINS RM, GOLDSMITH DJ, CONNOLLY J, SCOBLE JE, HENDRY BM, ACKRILL P, VENNING MC. Vasculitis and rapidly progressive glomerulonephritis in the elderly. Postgrad Med J [online] 1996 Jan, 72(843):41-44 [viewed 11 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2398323
  4. VALSON AT, SUNDARAM M, DAVID VG, DEBORAH MN, VARUGHESE S, BASU G, MOHAPATRA A, ALEXANDER S, JOSE J, ROSHAN J, SIMON B, REBEKAH G, TAMILARASI V, JACOB CK. Profile of incident chronic kidney disease related-mineral bone disorders in chronic kidney disease Stage 4 and 5: A hospital based cross-sectional survey Indian J Nephrol [online] 2014, 24(2):97-107 [viewed 11 September 2014] Available from: doi:10.4103/0971-4065.127897
  5. VIAZZI F, LEONCINI G, DERCHI LE, PONTREMOLI R. Ultrasound Doppler renal resistive index: a useful tool for the management of the hypertensive patient J Hypertens [online] 2014 Jan, 32(1):149-153 [viewed 11 September 2014] Available from: doi:10.1097/HJH.0b013e328365b29c
  6. STEVENS LA, CORESH J, SCHMID CH, FELDMAN HI, FROISSART M, KUSEK J, ROSSERT J, VAN LENTE F, BRUCE RD III, ZHANG Y(, GREENE T, LEVEY AS. Estimating GFR using Serum Cystatin C Alone and in Combination with Serum Creatinine: A Pooled Analysis of 3418 Individuals with CKD Am J Kidney Dis [online] 2008 Mar, 51(3):395-406 [viewed 13 September 2014] Available from: doi:10.1053/j.ajkd.2007.11.018
  7. NIKKEN JJ, KRESTIN GP. MRI of the kidney--state of the art Eur Radiol [online] 2007 Nov, 17(11):2780-2793 [viewed 13 September 2014] Available from: doi:10.1007/s00330-007-0701-3
  8. BAE KT, TAO C, ZHU F, BOST JE, CHAPMAN AB, GRANTHAM JJ, TORRES VE, GUAY-WOODFORD LM, MEYERS CM, BENNETT WM, AND CONSORTIUM FOR RADIOLOGIC IMAGING STUDIES POLYCYSTIC KIDNEY DISEASE (CRISP). MRI-based Kidney Volume Measurements in ADPKD: Reliability and Effect of Gadolinium Enhancement Clin J Am Soc Nephrol [online] 2009 Apr, 4(4):719-725 [viewed 13 September 2014] Available from: doi:10.2215/CJN.03750708
  9. CHAPMAN AB, WEI W. Imaging Approaches to Patients with Polycystic Kidney Disease Semin Nephrol [online] 2011 May, 31(3):237-244 [viewed 13 September 2014] Available from: doi:10.1016/j.semnephrol.2011.05.003
  10. ELLES RG, HODGKINSON KA, MALLICK NP, O'DONOGHUE DJ, READ AP, RIMMER S, WATTERS EA, HARRIS R. Diagnosis of adult polycystic kidney disease by genetic markers and ultrasonographic imaging in a voluntary family register. J Med Genet [online] 1994 Feb, 31(2):115-120 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1049671
  11. MERIKAS G, MARKETOS S, KONSTANTOPOULOS E. Uremic pericardial tamponade. Can Med Assoc J [online] 1966 Jul 16, 95(3):119-123 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1936728
  12. TUOT DS, PLANTINGA LC, HSU CY, JORDAN R, BURROWS NR, HEDGEMAN E, YEE J, SARAN R, POWE NR, FOR THE CENTERS FOR DISEASE CONTROL CHRONIC KIDNEY DISEASE SURVEILLANCE TEAM. Chronic Kidney Disease Awareness Among Individuals with Clinical Markers of Kidney Dysfunction Clin J Am Soc Nephrol [online] 2011 Aug, 6(8):1838-1844 [viewed 13 September 2014] Available from: doi:10.2215/CJN.00730111

Investigations - Fitness for Management

Fact Explanation
Full blood count Low haemoglobin is found due to the anaemia. [4] Anaemia in CKD is defined as an Hb level <13.5 g/dl in men and 12.0 g/dl in women. [1] There may be reduction in the mean corpuscular haemoglobin level and mean corpuscular volume, in association with the anaemia of chronic disease.
Blood picture There my be microcytic hypochromic blood picture or normocytic normochromic [3] blood picture due to the anaemia of chronic disease.
Serum ferritin level [1] Iron deficiancy could be either absolute or relative. Absolute iron deficiency is found when serum ferritin level <100 ng/ml or a transferrin saturation of <20%. Relative variety is where serum ferritin level ≥100 ng/ml and a reduction in iron saturation. [1]
Arterial blood gas analysis Metabolic acidosis is seen among CKD patients. [2]
Parathyroid hormone, phosphorus level and serum calcium level [3] Elevated parathyroid hormone and increaesd phosphorus level [3] is seen due to the secondary hyperparathyroidism. [3] Serum calcium may be normal or high due to the secondary hyperparathyroidism.
Fasting plasma glucose/HbA1c [7] Diabetes mellitus is an independent risk factor for the CKD. [7] Assessment of sugar level is important as a preoperative measure.
Electrocardigram Left-ventricular hypertrophy [1] , is found in association with heart failure. This LVH develops even in the mild stage of disease and progreeses as the disease progresses. [6]
Chest x-ray Preop assessment should includes chesy x-ray[8] particularly in patients with cardiac and respiratory problems.
Echocardiography, Chest radiographY, Pulmonary functions, noninvasive vascular studies, abdominal and renal ultrasonography, serologic tests for HIV infection, hepatitis B and hepatitis C, cytomegalovirus (CMV) infection, and other viral infections These tests are done prior to the kidney transplant [5] to assess the fitness for the procedure.
References
  1. MEHDI U, TOTO RD. Anemia, Diabetes, and Chronic Kidney Disease Diabetes Care [online] 2009 Jul, 32(7):1320-1326 [viewed 08 September 2014] Available from: doi:10.2337/dc08-0779
  2. MERIKAS G, MARKETOS S, KONSTANTOPOULOS E. Uremic pericardial tamponade. Can Med Assoc J [online] 1966 Jul 16, 95(3):119-123 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1936728
  3. THOMAS R, KANSO A, SEDOR JR. Chronic Kidney Disease and Its Complications Prim Care [online] 2008 Jun, 35(2):329-vii [viewed 09 September 2014] Available from: doi:10.1016/j.pop.2008.01.008
  4. KOSHY SM, GEARY DF. Anemia in children with chronic kidney disease Pediatr Nephrol [online] 2008 Feb, 23(2):209-219 [viewed 09 September 2014] Available from: doi:10.1007/s00467-006-0381-2
  5. WEBB N, JOHNSON R, POSTLETHWAITE R. Renal transplantation Arch Dis Child [online] 2003 Oct, 88(10):844-847 [viewed 09 September 2014] Available from: doi:10.1136/adc.88.10.844
  6. MITSNEFES MM. Cardiovascular Disease in Children with Chronic Kidney Disease J Am Soc Nephrol [online] 2012 Apr, 23(4):578-585 [viewed 09 September 2014] Available from: doi:10.1681/ASN.2011111115
  7. TARGHER G, CHONCHOL M, BERTOLINI L, RODELLA S, ZENARI L, LIPPI G, FRANCHINI M, ZOPPINI G, MUGGEO M. Increased Risk of CKD among Type 2 Diabetics with Nonalcoholic Fatty Liver Disease J Am Soc Nephrol [online] 2008 Aug, 19(8):1564-1570 [viewed 09 September 2014] Available from: doi:10.1681/ASN.2007101155
  8. KUMAR A, SRIVASTAVA U. Role of routine laboratory investigations in preoperative evaluation J Anaesthesiol Clin Pharmacol [online] 2011, 27(2):174-179 [viewed 13 September 2014] Available from: doi:10.4103/0970-9185.81824

Investigations - Followup

Fact Explanation
Haemoglobin Hb needs to be checked with the treatment for anaemia. Erythropoietin stimulating agents raise the level of haemoglobin by 1–2 g/dl over 4–8 week periods. [1]Hb level should be measured every other week initially and monthly thereafter. If there is increase in Hb more than 1g/dl within a 4-week period, thay can have increased risk for cardivasular events. [1] Hb levels >12 g/dl is associated with increased thrombotic events.
Serum creatinine , blood urea [3] and serum eletrolytes Impaired renal functions are associated with increased accumulation of waste products in the blood such as urea and creatinine. The most common and clinically significant electrolyte abnormality seen in chronic renal failure is hyperkalemia. [3] Hyponatremia, hypocalcemia, and hypermagnesemia may develop during the dialysis therapy.
Serum phosphorus level Should be maintained between 2.7 and 4.6 mg/dL in patients with stages 3 and 4 CKD, and between 3.5 and 5.5 mg/dL in individuals with stage 5. [2]
C reactive protein [2] Inflammation increases the CRP level. Elevated CRP can be used as a predictor for the outcome. [2]
References
  1. MEHDI U, TOTO RD. Anemia, Diabetes, and Chronic Kidney Disease Diabetes Care [online] 2009 Jul, 32(7):1320-1326 [viewed 08 September 2014] Available from: doi:10.2337/dc08-077
  2. THOMAS R, KANSO A, SEDOR JR. Chronic Kidney Disease and Its Complications Prim Care [online] 2008 Jun, 35(2):329-vii [viewed 09 September 2014] Available from: doi:10.1016/j.pop.2008.01.008
  3. MERIKAS G, MARKETOS S, KONSTANTOPOULOS E. Uremic pericardial tamponade. Can Med Assoc J [online] 1966 Jul 16, 95(3):119-123 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1936728

Investigations - Screening/Staging

Fact Explanation
Estimated GFR [1] Estimated GFR Ias used to stage the disease as mentioned above. Stage 1: normal eGFR ≥ 90 mL/min per 1.73 m2 and persistent albuminuria, stage 2: eGFR between 60 to 89 mL/min per 1.73 m2, stage 3: eGFR between 30 to 59 mL/min per 1.73 m2, stage 4: eGFR between 15 to 29 mL/min per 1.73 m2, and stage 5: eGFR of < 15 mL/min per 1.73 m2. [1]
References
  1. THOMAS R, KANSO A, SEDOR JR. Chronic Kidney Disease and Its Complications Prim Care [online] 2008 Jun, 35(2):329-vii [viewed 09 September 2014] Available from: doi:10.1016/j.pop.2008.01.008

Management - General Measures

Fact Explanation
Patient education As the patient is vulnerable for lot of complications they should be told about the potential complications, available treatment options including renal replacement therapy. [2]
Physical activity [3] American College of Sports Medicine and American Heart Association, recomends that risk of cardiovascular events, in individuals with chronic illnesses can be reduced by performing moderate-intensity physical activity, 30 min, 5 times weekly. [3]
Diet and nutrition [1] These patients are vulnerable for malnutrition due to the inadequate nutrient intake and ineffective nutrient utilization. Uremic malnutrition, is a state develops due to the poor dietary intake. [1] Serum prealbumin levels less than 30 mg/dL suggest protein depletion. Restriction of dietary phosphorus is advised when phosphate or parathyroid hormone levels begin to rise. [1] Potassium level affects the ingestion of fruits and vegetables.
Vitamin supplimentation Supplementation with calciferols is recomended in CKD patients with low vitamin D levels. [6] Supplementation of 25-(OH)-vitamin D is required initially and calcitriol replacement is needed in Stage 3. [5] Hyperhomocysteinemia is a risk factor for atheresclerosis in these patients and therefore pyridoxine and folic acid supplementaion is useful in CKD patients.
Symptomatic management Cardiovascular diseases are the leading causes of death in patients with CKD, particularly in patients with diabetes. [4] Heart failure and pulmonary oedema are potential complications in these patients. Respiratory tract infections are also common. Hiccups may need treatment with ranitidine.
References
  1. THOMAS R, KANSO A, SEDOR JR. Chronic Kidney Disease and Its Complications Prim Care [online] 2008 Jun, 35(2):329-vii [viewed 09 September 2014] Available from: doi:10.1016/j.pop.2008.01.008
  2. MAGOR AM, WARBURTON J, TROWER MK, GRIFFIN M. Comparative Study of the Ability of Three Xanthobacter Species To Metabolize Cycloalkanes Appl Environ Microbiol [online] 1986 Oct, 52(4):665-671 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC239094
  3. SHIRAISHI FG, STRINGUETTA BELIK F, OLIVEIRA E SILVA VR, MARTIN LC, HUEB JC, GONçALVES RD, CARAMORI JC, BARRETI P, FRANCO RJ. Inflammation, Diabetes, and Chronic Kidney Disease: Role of Aerobic Capacity Exp Diabetes Res [online] 2012:750286 [viewed 09 September 2014] Available from: doi:10.1155/2012/750286
  4. TARGHER G, CHONCHOL M, BERTOLINI L, RODELLA S, ZENARI L, LIPPI G, FRANCHINI M, ZOPPINI G, MUGGEO M. Increased Risk of CKD among Type 2 Diabetics with Nonalcoholic Fatty Liver Disease J Am Soc Nephrol [online] 2008 Aug, 19(8):1564-1570 [viewed 09 September 2014] Available from: doi:10.1681/ASN.2007101155
  5. WILLIAMS S, MALATESTA K, NORRIS K. Vitamin D and Chronic Kidney Disease Ethn Dis [online] 2009, 19(4 Suppl 5):S5-8-11 [viewed 13 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878736
  6. KANDULA P, DOBRE M, SCHOLD JD, SCHREIBER MJ JR, MEHROTRA R, NAVANEETHAN SD. Vitamin D Supplementation in Chronic Kidney Disease: A Systematic Review and Meta-Analysis of Observational Studies and Randomized Controlled Trials Clin J Am Soc Nephrol [online] 2011 Jan, 6(1):50-62 [viewed 13 September 2014] Available from: doi:10.2215/CJN.03940510

Management - Specific Treatments

Fact Explanation
Management of anaemia [1] Hb target in CKD patients is usually 11–12 g/dl and should not exceed 13 g/dl. [1] It should be individualized treatment depending on the symptoms, and Hb level.Initially the underlying cause for the anaemia needs to be evaluated. Absolute iron deficiency is treated with either oral or intravenous iron therapy. Eg:- Oral ferrous gluconate, fumarate, and sulfate and intravenous iron dextran, ferric sodium gluconate, iron sucrose, if they are not tolerating the oral preparations due to the side effects. [1] Erythropoietin stimulting agents/ recombinant human erythropoietin (epo) [2] such as epoetin-α 10,000 units once weekly or darbepoetin-α 0.75 μg/kg every other week subcutaneously are also effective in the treatment of anaemia, and these agents raise the level of haemoglobin by 1–2 g/dl over 4–8 week periods. [1] Dosing interval may be adjusted from weekly to once monthly according to the response. These agents increase the risk of hypertension and therefore is not recomended to use in patients with uncontrolled blood pressure. [1] [2]
Management of bone disease [4] As the secondary hyperparathyroidism develops, serum phosphate level will rise with distortion of the bone architecture. This bone ditortion can happen even when the serum phosphorus lees are normal, therefore phosphate binders are recomended to start when eGFRs is below 50 mL/min per 1.73 m2. [2] Aluminium based, calcium based phosphate binders are available. There is new one called nonabsorbable agent sevelamer which is calcium and aluminium free. [2] Vitamin D and calcimimetics will suppress parathyroid hormone secretion. Calcimimetics down-regulates the parathyroid hormone secretion and reducing hyperplasia of the parathyroid gland. [2,4]
Management of metabolic acidosis Metabolic acidosis in patients with chronic kidney disease is due to the lack of tubular bicarbonate production, that is important to neutralizes the acid net production. [9] This acidosis will further contributes to the decline in renal function. Oral supplementation of the bicarbonate therefore reduces the progression of deterioration. [9]
Management of hypercalcemia [10] Intravenous bisphosphonates areused for the initial management of hypercalcaemia, and treatment can be continuedwith oral, drugs to prevent relapses. [11]
Management of proteinuria [3] Reduction of intraglomerular pressure and thus the proteinuria, can be achieved by ACEI inhibitors and angiotensin 2 receptor blockers. They also diminish the local release of cytokines, chemokines and activation of inflammatory pathways, and reduce the glomerular hypertrophy and sclerosis, tubulointerstitial inflammation, and fibrosis. [3]
Management of hyperurecemia [5] Patients with CKD can develop hyperuricemia as the disease progresses withreduction in the GFR. Allopurinol has shown to be effective in the management of hyperurecemia. [5]
Management of cormorbidities [2] Hypertension, hyperlipidaemia, heart disease and diabetes mellitus need to be well contorlled to acheive retardation of the disease progression in CKD. [2] Diabetes is associated with adverse outcomes in all stages of CKD.
Management of cardiovascular problems Blood pressure control is done with a target blood pressure of less than 130/85 mm Hg for all patients with kidney disease and less than 125/75 mmHg for patients with urinary protein excretion greater than 1g/24h. [2] Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers, are the first-line agents in patients with proteinuric (> 1 gm/24h), progressive diabetic and nondiabetic renal disease as they have recognized renal protective effect. [2] Calcium-channel blockers except dihydropyridine type and beta-blockers are are safe and often combination therapy may be needed when blood pressure is >160/100 mmHg in adults. [3]
Management of dyslipidaemia Patients with LDL cholesterol levels between 100 and 129 mg/dL are initially put on lifestyle changes, failing which a low-dose statin therapy is started. Patients with LDL ≥ 130 mg/dL can be started on low dose of statin, and patients with TG ≥ 200 mg/dL, low dose statin which is increased as needed to achieve target levels is recomended. [2]
Renal replacement therapy [6] Renal replacement therapy comprised of dialysis and kidney transplant. [6] Peritoneal dialysis (PD) and hemodialysis (HD) are the methods of dialysis. Renal transplant may be either live related or unrelated donor or cadeveric transplant.
Dialysis [7] There are main two types of dialysis :peritoneal dialysis (PD) and hemodialysis (HD). [7] Vascular access type of HD using an arteriovenous fistula (AVF) or an arteriovenous graft (AVG) is significantly associated with patient survival. but central venous catheters are associated with greater risk of sepsis, and mortality. Electrolyte imbalances, infections, dialysis equlibrium syndrome, and haemorrhage are the potential complications of the dialysis. Acidosis, Changes in calcium and phosphorus metabolism, lipid disorders, serositis, pericarditis, gout, pseudogout, impotence, infertility, spontaneous abortion and arteriovenous malformations are the other less frequent complications due to the treatment of dislysis.
Kidney transplant [6] Renal transplantation is indicated for the patients with endstage renal failure. This will eliminate the need for time consuming, disterssing treatment options and may be more comfortable to the patient. [8] It may be live donor or cadeveric transplant and live donor may be either related or unrelated. [8] Younger donor and recipient age, reduced cold ischaemia time and well matched HLA reduces the risk of rejection of the transplant. [8] Cyclosphorine based triple therapy (cyclosphorine combined with azathioprine and corticosteroids)is usually used as the immunosuppresants after the surgery. It has to be lifelong. Metastatic cancer, ongoing or recurring infections, serious cardiac or peripheral vascular disease, hepatic insufficiency is some of the contraindications to renal transplant.
References
  1. MEHDI U, TOTO RD. Anemia, Diabetes, and Chronic Kidney Disease Diabetes Care [online] 2009 Jul, 32(7):1320-1326 [viewed 08 September 2014] Available from: doi:10.2337/dc08-077
  2. THOMAS R, KANSO A, SEDOR JR. Chronic Kidney Disease and Its Complications Prim Care [online] 2008 Jun, 35(2):329-vii [viewed 09 September 2014] Available from: doi:10.1016/j.pop.2008.01.008
  3. WüHL E, SCHAEFER F. Therapeutic strategies to slow chronic kidney disease progression Pediatr Nephrol [online] 2008 May, 23(5):705-716 [viewed 09 September 2014] Available from: doi:10.1007/s00467-008-0789-y
  4. WILLIAMS S, MALATESTA K, NORRIS K. Vitamin D and Chronic Kidney Disease Ethn Dis [online] 2009, 19(4 Suppl 5):S5-8-11 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878736
  5. GOICOECHEA M, DE VINUESA SG, VERDALLES U, RUIZ-CARO C, AMPUERO J, RINCóN A, ARROYO D, LUñO J. Effect of Allopurinol in Chronic Kidney Disease Progression and Cardiovascular Risk Clin J Am Soc Nephrol [online] 2010 Aug, 5(8):1388-1393 [viewed 09 September 2014] Available from: doi:10.2215/CJN.01580210
  6. MAGOR AM, WARBURTON J, TROWER MK, GRIFFIN M. Comparative Study of the Ability of Three Xanthobacter Species To Metabolize Cycloalkanes Appl Environ Microbiol [online] 1986 Oct, 52(4):665-671 [viewed 09 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC239094
  7. PERL J, WALD R, MCFARLANE P, BARGMAN JM, VONESH E, NA Y, JASSAL SV, MOIST L. Hemodialysis Vascular Access Modifies the Association between Dialysis Modality and Survival J Am Soc Nephrol [online] 2011 Jun, 22(6):1113-1121 [viewed 09 September 2014] Available from: doi:10.1681/ASN.2010111155
  8. WEBB N, JOHNSON R, POSTLETHWAITE R. Renal transplantation Arch Dis Child [online] 2003 Oct, 88(10):844-847 [viewed 09 September 2014] Available from: doi:10.1136/adc.88.10.844
  9. GAGGL M, CEJKA D, PLISCHKE M, HEINZE G, FRAUNSCHIEL M, SCHMIDT A, HöRL WH, SUNDER-PLASSMANN G. Effect of oral sodium bicarbonate supplementation on progression of chronic kidney disease in patients with chronic metabolic acidosis: study protocol for a randomized controlled trial (SoBic-Study) Trials [online] :196 [viewed 13 September 2014] Available from: doi:10.1186/1745-6215-14-196
  10. BHAN I, DUBEY A, WOLF M. Diagnosis and Management of Mineral Metabolism in CKD J Gen Intern Med [online] 2010 Jul, 25(7):710-716 [viewed 13 September 2014] Available from: doi:10.1007/s11606-010-1316-y
  11. RALSTON SH. Medical management of hypercalcaemia. Br J Clin Pharmacol [online] 1992 Jul, 34(1):11-20 [viewed 13 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1381369