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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2008  |  Volume : 19  |  Issue : 4  |  Page : 669-677
Dilemma of Renal Disease in Elderly

1 Nephrology Unit, New Damietta Al-Azhar University Hospital and Faculty of Medicine, Mansoura Urology and Nephrology Center, Mansoura, Egypt
2 Department of Nephrology, Armed Forces Hospital, Riyadh, Saudi Arabia

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The aging process results in profound anatomic and functional changes in a number of human body systems. Changes in kidney function with normal aging are the most dramatic of any human organ or organ system. These include anatomical, physiological, hemodynamic and immunological changes. Increased propensities of systemic diseases and exposure to poly-pharmacy of the aged group have an additive deleterious effect. The aforementioned changes have its implications on clinical presentations, management and prognosis of all renal diseases in elderly. Atypical presentation, more frequent and longer course are the characteristics of acute renal failure in this age group. Also, presentation of glomerular diseases, clinical course, prognosis, decision of performing a renal biopsy and use of immunosuppressive drugs in elderly specially those subgroup above 80 years of age are still a big challenges that needs a consensus and standardization.

How to cite this article:
El Essawy AB, Mousa D, Al-Sulaiman M. Dilemma of Renal Disease in Elderly. Saudi J Kidney Dis Transpl 2008;19:669-77

How to cite this URL:
El Essawy AB, Mousa D, Al-Sulaiman M. Dilemma of Renal Disease in Elderly. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2022 Nov 28];19:669-77. Available from: https://www.sjkdt.org/text.asp?2008/19/4/669/41337

   Introduction Top

Membrano-Proliferative Glomerulonephritis (MPGN) is an uncommon cause of glome­rular disease that, in its idiopathic form, primarily occurs between the ages of 8 and 30 years. [1],[2],[3] It was reported to be between 2.6-4.9% among elderly with glomerular disease. [4],[5],[6],[7] Acute renal failure (ARF) has been reported as a complication in patients with minimal change and focal segmental glomerulosclerosis with increased risk in males, older individuals, and those with hypertension, lower serum albumin levels and greater proteinuria. [8],[9],[10] ARF has rarely been described in patients with membra­nous nephropathy. [11] We report an elderly patient with MPGN presented initially with ARF.

   Case Presentation Top

An 81-year-old man who is a known case of well controlled hypertension by angioten­sin receptor type 1 (AT1-R) blockers, Osteo­arthritis on non-steroidal anti-inflammatory drug (NSAID) and dyslipidemia controlled by atorvastatin 60 mg daily. The patient presented to the emergency with easy fati­gability and confusion. The patient was alert and conscious. His Weight was 76 kg, Blood pressure 182/73 mmHg, Oxygen saturation 95-97% in room air. Tempera­ture was 36.4°C. There was no neurolo­gical deficit and systemic examination was unremarkable.

Laboratory results showed blood urea 24.2 mmol/L, serum creatinine 643 µmol/L, Na 138, K 4.2 mmol/L, random blood glu­cose 6.1 mmol/L, total protein 59 g/L, albumin 39 g/L, alkaline phosphatase 103 U/L and ALT 63 U/L, WBCs on admission 7000, hemoglobin 10.9 g/dl, platelets 247 and 24 hours proteinuria (PU) was 1.9 g/d. Liver, thyroid function tests, ESR and C reactive protein were normal. Chest X ray and KUB were unremarkable. Renal U/S revealed normal sized echogenic kidneys with no evidence of obstruction while the small benign hyperplastic prostate was al­ready under alpha 1 receptor blocker as a medical treatment. There was no clinical evidence of pre-renal ARF on presentation. To further clarify the nature of the ARF; glomerulnephritis screen was carried out and revealed negative (ANA, anti-ds-DNA, CRP, C3, C4, serum and urine immunoelectropho­resis, serum immunoglobulin, HCV, HbsAg). Tumor markers, CEA, Ca19-9 and PSA revealed negative. Only CK and LDH re­vealed 3020 and 653 U/L respectively while the other cardiac enzymes were normal. Urine showed both glomerular and non glo­merular RBCs and proteinuria.

Our initial differential diagnosis was

  1. Interstitial nephritis due to NSAID? and/or
  2. Rhabdomyolysis due to atorvastatin therapy?

So the treatment was

  1. Stop both atrovastatin and NSAID and
  2. Intravenous fluids and daily laboratory follow-up

Patient showed marked improvement and discharged after 3 weeks of conservative management with: S Cr 149 µmol/L, blood urea 14.4 mmol/L, Albumin 33 g/L, CK 109 U/L and LDH 275 U/L. But 24 hour PU which was 1.9 g/d on admission went up to 15.5 g/d on discharge. Our debate conclu­ded to discharge the patient without renal biopsy on antiproteinuric measures (AT1­R blockers) and tight follow up.

Two months after discharge his S Cr went up from 149 to 266 µmol/L; 24 h PU was 11.04 g/d, both glomerular and non-glome­rular haematuria, S Cholesterol 10 mmol/L, serum albumin went down to 24 g/L and pa­tient developed moderate lower limb edema.

So renal biopsy was carried out which revealed a MPGN on a back ground of interstitial fibrosis and tubular atrophy in addition to arteriolar hypertensive changes [Figure 1],[Figure 2],[Figure 3],[Figure 4],[Figure 5],[Figure 6]. Again after a debate the pa­tient was discharged on a prednisolone 60 mg and cyclosphosamide on a modified dose of 1 mg/kg.

   Case Revisited Top

Patient was followed in out patient clinic on a weekly basis for the first month then biweekly afterward. After 4 weeks of treatment patient showed initial improvement with S Cr 128 µmol/l, albumin 28 g/l, the 24 h PU 5.7 g/d (> 50% reduction) while the total cholesterol still 12.3 mmol/L as the antilipidemics were stopped due to the high creatine kinase on initial presentation. Two weeks later patient presented with severe chest infection associated with an ARF with RIFLE criteria as failure (Risk, Injury, Failure, Lost and End stage). Patient was re-hospitalized and treated with the appro­priate antibiotics, while his renal function kept deteriorating. ICU admission and con­tinuous renal replacement therapy (CRRT) was done for three days followed by inter­mittent dialysis through a central catheter (permicath). Once the infection subsided (2 weeks after admission) patient was dis­charged to continue his dialysis 3 times weekly on outpatient basis and follow up his renal profile. One week later the patient readmitted again for a venous line related sepsis. After a total of 8 weeks on dialysis from the 2nd episode of ARF and proper management, the patient discharged off dialysis with a S Cr of 300 µmol, Albumin of 27 g/L, cholesterol of 3.4 mmol/L and 24 h PU of 4.4 g/d on a combination of antiproteinuric (ACE inhibitors and AT1-R Blockers), lipid lowering drugs and anti­platelets [Table 1].

   Discussion Top

Acute renal failure in elderly

ARF is a frequent disorder in the old population and the increased incidence of this renal syndrome in this age group is favored by some factors such as the histo­logical and functional changes of the aged kidney, the reduced capability of this po­pulation to metabolize drugs, and their exposure to polypharmacy and to a great number of systemic diseases such as dia­betes mellitus, hypertension and cardiac fai­lure. [12] Among the main senile renal changes that make old people prone to acute renal failure are:

  1. Disturbance in the auto-regulatory vas­cular defense. [13]
  2. A reduction in the number of glomeruli and glomerular capillaries. [13]
  3. Their renal tubular fragility. [14]
  4. A salt and water wasting secondary to a reduced tubular reabsorption capabi­lity of these substances. [15]

Our patient proved to have hypertension for many years, age related osteoarthritis treated by NSAID and hyperlipidemia trea­ted by atorvastatin. All these are inde­pendent risk factors and/or cause of ARF. His elevated serum level of CK and LDH at presentation raised the question of asso­ciated drugs related rhabdomyolysis espe­cially with atorvastatin.

The patient presented to the emergency with complaints of easy fatigability and confusion without any nephrological symp­toms. Atypical presentations of the ARF in elderly have been clearly reported. [16],[17],[18],[19] In the elderly, the diseases usually have pat­terns of presentation different to the ones observed in the young population (pauci­syntomatic). Signs and symptoms are fre­quently less defined in the age population. Moreover, any disease could appear merely as one of the entities known as the geria­trics giants: confusional syndrome, falls, im­mobility syndrome and acute urinary or fecal incontinence. These presentation pat­terns are called "atypical" but actually they are "typical" in this population. [16],[17],[18],[19]

In additions, due to the convinced in­fluence of the senile tubular frailty and tubular dysfunction, in old people is fre­quently observed the so called "interme­diate syndrome", it means a patient suffe­ring from a pre-renal acute renal failure who seems to be suffering from a paren­chymal one since this old patient usually has not only high plasma urea and crea­tinine but also urinary indices compatible with acute tubular necrosis. However, they resolve the renal failure with volume ex­pansion as a pre-renal insufficiency does. However, while the classical pre-renal failure recovers in 24-48 hours of rehydra­tion, the intermediate syndrome does it in a longer period. [20]

Acute renal failure as a complication of nephrotic syndrome

ARF is a known complication of patient with nephrotic syndrome mostly with mi­nimal change disease (MCD) 5% of cases, while focal segmental glomerulosclerosis (FSGS) only represent 8% of cases spe­cially the collapsing FSGS which usually associate the HIV disease. Membranous nephropathy is rarely complicated by ARF while diabetic nephropathy and amylodo­sis is very unusual. An increased risk noted in males, older individuals, and those with hypertension, lower serum albumin levels and greater proteinuria.

However, ARF usually happen as a com­plication of nephrotic syndrome or its treat­ment. It is quite uncommon that the first presentation, as in our case, of nephrotic and nephritic syndrome mainly membrano­ proliferative GN to be ARF. [21],[22]

Membranoproliferative GN

The outcome is generally not so good in patients with apparently idiopathic MPGN. Up to 50-60 % of untreated patients will progress to ESRD within 10-15 yrs. 25-40 % will maintain apparently normal renal func­tion. Spontaneous improvement occurs in < 10 % of cases. Bad prognostic signs at presentation include:

  1. The nephrotic syndrome.
  2. Renal insufficiency.
  3. Hypertension.
  4. On renal biopsy, crescents, tubulointers­ titial disease (interstitial infiltration and fibrosis, tubular atrophy).

The risk of progression usually correlates more closely with the severity of the tubu­lointerstitial injury than with the degree of glomerular damage. The long-term prog­nosis tends to be relatively good in patients who present with asymptomatic hematuria and proteinuria and who have focal, rather than diffuse, glomerular involvement on renal biopsy. [23],[24],[25],[26],[27],[28],[29] Our patient despite he presen­ted with ARF, he has both hematuria and proteinuria without casts. As his renal func­tion improved, his proteinuria dramatically increased with the appearance of the cardi­nal manifestation of glomerular disease which proved to be MPGN on renal biopsy.

Immunosuppressive therapy in elderly

Immunosenescence describes an increa­singly insufficient function of the immune system that increases the susceptibility of the elderly toward infection, autoimmune disease, and cancer, contributing significantly to morbidity and mortality. [30],[31] The immune system undergoes a complex and continuous remodeling as a result of aging. Both volume and mass of virtually all solid lym­phoid organs become smaller. These changes are paralleled by age-related morphologic changes of the immune system (blurring of histologic architecture, fatty infiltration, fib­rosis, and reduction of germinal centers) in addition to functional alterations. [32]

These age-related changes result in both quantitative and qualitative modifications with increased, decreased, and unchanged functions of specific subsystems, rather than a global deterioration of the immune system as previously believed. [33],[34] The most striking alterations are found in phe­notypes and functions of T-cell compo­nents and less frequently in components of the natural (innate) immune system. Con­sequently, chemotaxis, phagocytosis, natural cytotoxicity, and complement activity are relatively well preserved in elderly indi­viduals. [35] Alterations of B cells seem to be secondary to T-cell dysfunction. [31]

A greater degree of immunosuppression (IS) results in an increased risk of infec­tious complications in all patients (young and old). However, as previously mentioned, immunocompetence decreases with age; as a result, older individuals are more suscep­tible to infectious complications at lower levels of immunosuppressive therapy. In addition, increased incidence of associated co-morbidities and altered pharmacokinetics make prescribing immunosuppressive me­dications in the elderly a very challenging issue. Consequently, modifications of the immune system because of aging may request an age-adapted immunosuppression in parallel with close patient monitoring. [36]

After a debate about using the standard immunosuppressive treatment in MPGN in elderly above 80 yrs of age; patient re­ceived steroid and modified dose of cyclo­phosphamide. After initial improvement de­fined as more than 50 % reduction in the PU, increased serum albumin and improve­ment of kidney function. Patients develop two subsequent episodes of septicemia with ARF. After stoppage of IS, patient needed to be hospitalized for a total of three weeks. So, the benefit of using IS in old man was counteracted by the infectious com­plications that lead to ARF and long time hospitalization. So, the question is: is there is a place to use aggressive IS in elderly above the age of 80ys.

   Conclusion Top

MPGN can present initially as ARF. Is it wise to start an aggressive IS therapy in elderly patient above 80 yrs old even in a modified doses. Is there any standardization regarding the dose and type which guide the use of IS in elderly.

Further prospective studies are necessary to address this issue.

   Questions and Answers Top

Dr. Akram Askar (King Khaled Univer­sity Hospital, Chairman of the RNTC): the presentation is now open for discussion.

Dr. Mohammad Ziad Souqiyyeh (SCOT): When somebody present with proteinuria usually above the age of 40 years, we do urine immuno electropheresis, just to see if the patient has multiple myeloma. Was that done?

Speaker: Yes. Actually the patient presented as ARF with creatinine over 600 umol/L, without any previous medical record, and during initial investigation the proteinuria was 1.9 g/24 hrs. and in our differential diagnosis we consider the acute interstitial nephritis because of the history of non-steroidal anti­inflammatory drugs for long period with long standing hypertension and he is receiving anti-lipid drugs, so all these together give the picture of systemic disease affecting the kidneys.

Dr. Souqiyyeh: But later on, he presented with heavy proteinuria and my question is why the renal biopsy was not done at the first presentation?

Speaker: Your point is valid, for any patient presented with proteinuria, but here the scenario is different that our patient is over 80 years old presented with ARF, can be due to interstitial nephritis, and we give him the chance to recover his renal function, and the most interesting that once his renal function was restored, the proteinuria in­creased to as 15 g/24 hrs, and here we did the biopsy, with the debate of to do biopsy or not? And to treat the patient or not?

Dr. Souqiyyeh: My last comment on immu­nosuppressive therapy, usually in younger patient with such finding, we apply full re­gimen of immunosuppressive drugs; here in this case what was your therapeutic plan?

Speaker: We gave the patient 50 mg of cyclophospamide (1/2 of the usual dose) plus 60 mg of steroids daily, during this course patient developed a second attack of ARF mostly precipitated by sepsis, which indi­cated starting the dialysis therapy.

   References Top

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2.Cameron JS, Turner DR, Heaton J, et al. Idiopathic mesangiocapillary glomerulo­nephritis: comparison of types I and II in children and adults and long-term prog­nosis. Am J Med 1983;74:175.  Back to cited text no. 2  [PUBMED]  
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5.Kingswood JC, Banks RA, Tribe CR, Owen-Jones J, Mackenzie JC. Renal biopsy in the elderly: clinicopathological corre­lations in 143 patients. Clin Nephrol 1984; 22:183.  Back to cited text no. 5  [PUBMED]  
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7.Kaneda K, Taguchi S, Yanase K, et al. Clinicohistopathological studies of glome­rular disease in 185 elderly patients aged over 60. Jin to Tohseki 1990;28:929.  Back to cited text no. 7    
8.Smith JD, Hayslett JP. Reversible renal failure in the nephrotic syndrome. Am J Kidney Dis 1992;19(3):201-13.  Back to cited text no. 8    
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10.Waldman M, Crew RJ, Valeri A, et al. Adult minimal-change disease: clinical characteristics, treatment, and outcomes. Clin J Am Soc Nephrol 2007;2(3):445-53.  Back to cited text no. 10    
11.Kunis CL, D'Agati V, Appel GB. Acute renal failure (ARF) in idiopathic nephrotic syndrome (NS). J Am Soc Nephrol 1997; 8:126A.  Back to cited text no. 11    
12.Lameire N, Nelde A, Hoeben H, Vanholder R. Acute renal failure in the elderly. In: Oreopoulos D, Hazzard W, Luke R, eds. Nephrology and Geriatrics integrated. Dordrecht: Kluwer Academic Publishers; 2000:93-111.  Back to cited text no. 12    
13.Hernando Avendano L, Lopez Novoa J. Glomerular filtration and renal blood flow in the aged. In: Macias Nunez JF, Cameron S, eds. Renal function and di­sease in the elderly. London: Butterworth; 1987: 27.  Back to cited text no. 13    
14.Musso CG. Geriatric nephrology and the 'nephrogeriatric giants'. Int Urol Nephrol 2002;34:255.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Macias Nunez JF, Garcia Iglesias C, Bondia Roman A, et al. Renal handling of sodium in old people: a functional study. Age Ageing 1978;7:178.  Back to cited text no. 15    
16.Perez Almeida E, Blanco Pascual E. The patient with immobility syndrome. In: Macias Nunez JF, Guillen Llera FG, Ribera Casado JM, eds. Geriatrics from the bigining. Barcelona: Editorial Glosa; 2000. p. 135.  Back to cited text no. 16    
17.Verdejo Bravo C. The patient with incon­tinente sindrome. In: Macias Nunez JF, Guillen Llera FG, Ribera Casado JM, eds. Geriatrics from the beginning. Barcelona. Editorial Glosa, 2000;153.  Back to cited text no. 17    
18.Lazaro del Nogal M. The patient with gait disorders and falls. In: Macias Nunez JF, Guillen Llera FG, Ribera Casado JM, eds. Geriatrics from the beginning. Barcelona. Editorial Glosa, 2000;166.  Back to cited text no. 18    
19.Gil Gregorio P. The patient with psychia­tric alterations. In: Macias Nunez JF, Guillen Llera FG, Ribera Casado JM, eds. Geriatrics from the bigining. Barcelona. Editorial Glosa, 2000;183.  Back to cited text no. 19    
20.Musso CG. Intermediate syndrome: atypical pattern of acute renal failure in elderly. Electron J Biomed 004;3:33. Available from: 2004/ n3/ musso-en.html  Back to cited text no. 20    
21.Jennette JC, Falk RJ. Adult minimal change glomerulopathy with acute renal failure. Am J Kidney Dis 1990;16(5):432-7.  Back to cited text no. 21    
22.Waldman M, Crew RJ, Valeri A, et al. Adult minimal-change disease: clinical characteristics, treatment, and outcomes. Clin J Am Soc Nephrol 2007;2(3):445-53.  Back to cited text no. 22    
23.D'Amico G, Ferrario F. Mesangio-capil­lary glomerulonephritis. J Am Soc Nephrol 1992;2(10):S159-66.  Back to cited text no. 23    
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25.Cameron JS, Turner DR, Heaton J, et al. Idiopathic mesangiocapillary glomerulo­nephritis: Comparison of types I and II in children and adults and long-term prog­nosis. Am J Med 1983;74:175.  Back to cited text no. 25  [PUBMED]  
26.Schena FP, Cameron JS. Treatment of proteinuric glomerulonephritides in adults. Am J Med 1988;85:315.  Back to cited text no. 26  [PUBMED]  
27.Little MA, Dupont P, Campbell E, et al. Severity of primary MPGN, rather than MPGN type, determines renal survival and post-transplantation recurrence risk. Kidney Int 2006;69(3):504-11.  Back to cited text no. 27    
28.Bennett WM, Fassett RG, Walker RG, Fairley KF, d'Apice AJ, Kincaid-Smith P. Mesangiocapillary glomerulonephritis type II (dense-deposit disease): Clinical features of progressive disease. Am J Kidney Dis 1989;13(6):469-76.  Back to cited text no. 28    
29.McEnery PT, McAdams AJ. Regression of membranoproliferative glomerulonephritis type II (dense deposit disease): Obse­rvations in six children. Am J Kidney Dis 1988;12(2):138-46.  Back to cited text no. 29    
30.Pawelec G. Immunosenescence: Impact in the young as well as the old? Mech Ageing Dev 1999;108(1):1-7.  Back to cited text no. 30    
31.Castle SC. Clinical relevance of age­related immune dysfunction. Clin Infect Dis 2000;31(2):578-85.  Back to cited text no. 31    
32.Powers DC, Nagel JE, Adler WH. Immuno­logical changes in the elderly. In: Katlic MR, ed. Geriatric surgery: com-prehensive care of the elderly. Baltimore, Urban & Schwarzenberg, 1990;173.  Back to cited text no. 32    
33.Ginaldi L, DeMartinis M, D' Ostilio A, Marini L, Loreto MF, Quaglino D. Immunological changes in the elderly. Aging (Milano) 1999;11(5):281-6.  Back to cited text no. 33    
34.Globerson A, Effros RB. Ageing of lymphocytes and lymphocytes in the aged. Immunol Today 2000;21(10):515-21.  Back to cited text no. 34    
35.Cossarizza A, Ortolani C, Monti D, Fran­ceschi C. Cytometric analysis of immuno­senescence. Cytometry 1997;27(4):297-313.  Back to cited text no. 35    
36.Martins PN, Pratschke J, Pascher A, et al. Age and immune response in organ transplantation. Transplantation 2005;79(2): 127-32.  Back to cited text no. 36    

Correspondence Address:
Mohamed Al-Sulaiman
Department of Nephrology, Riyadh Armed Forces Hospital, Riyadh
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

PMID: 18580035

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