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Decreased Kidney Function in the Elderly: Clinical and Preclinical, Neither Benign

Josef Coresh, MD, PhD; and Brad Astor, PhD
[+] Article, Author, and Disclosure Information

From Johns Hopkins University, Baltimore, MD 21287.

Potential Financial Conflicts of Interest: None disclosed.

Grant Support: Drs. Coresh and Astor are partly supported by 5U01DK067651.

Requests for Single Reprints: Josef Coresh, MD, PhD, Johns Hopkins University, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21287; e-mail, coresh@jhu.edu.

Current Author Addresses: Drs. Coresh and Astor: Johns Hopkins University, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21287.

Ann Intern Med. 2006;145(4):299-301. doi:10.7326/0003-4819-145-4-200608150-00010
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Decreased kidney function is extremely common in elderly persons and is also an important independent predictor of cardiovascular disease. An advance in detecting decreased kidney function and quantifying its prognostic and therapeutic implications is, therefore, important news for clinicians. In this issue, Shlipak and colleagues (1) advance our understanding of the broad consequences of mildly decreased kidney function in elderly persons. They also demonstrate that cystatin C has some advantages over serum creatinine as a marker of decreased glomerular filtration rate (GFR) in predicting future complications.

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Posted on October 3, 2006
Carlos Musso
Hospital Italiano
Conflict of Interest: None Declared

To the Edditor,

We read with interest the editorial by Dr. Coresh and Dr. Astor (1) regarding the reduction in senile glomerular filtration rate (GFR) and its potential interpretation as an incipient chronic kidney disease (CKD).

However we would like to emphasize that although the aged kidney has a decreased GFR, it differs in a number of ways from the kidney with chronic renal failure, which the physician should keep in mind when treating these patients. Thus the healthy person (older than 75 years) and patients with chronic kidney disease (stage 3) share two main physiological characteristics: 1) a similar glomerular filtration rate (about 50 mL/min per 1.73 m² ), and 2) a diminished capability for salt and water reabsorption from the renal tubule (2,3). Despite of these similarities, the aged kidney and the chronically damaged one differ markedly in many other physiological aspects:

-Proximal tubular function is perfectly preserved in the healthy oldest old and their serum erythropoietin and haemoglobin levels are normal. Conversely, anemia secondary to a low serum erythropoietin secretion is one of the main characteristics in CKD patients (4,5,6,7).

-Even though the fractional excretion of urea is increased in both settings, serum urea level is normal in the elderly while it is increased in chronic nephropathy (6,8).

-Serum levels and fractional excretion of magnesium, calcium and phosphorus are normal in the healthy very old population, while CKD patients usually have increased fractional excretion of these substances, in the presence of a normal magnesium, low calcium, and high phosphorus serum levels. Parathyroid hormone and active vitamin D levels are normal in the healthy oldest old, while the former is increased and the latter is decreased in the CKD population (3,9,10). -Regarding potassium excretion, in chronic nephropathy the fractional excretion of potassium increases as GFR decreases under the influence of the aldosterone hormone. However, the fractional excretion of potassium is relatively diminished in relationship to GFR in the healthy very old people. This phenomenon has been attributed to a tubular resistance to aldosterone in this age group and in these patients frequently can lead to hyperkalcemia (3, 11,12).

As a result of the differences described above, even though the aged kidney can be considered as a "sick" organ, the decreased GFR has a different significance compared to the state that currently we refer to as chronic renal disease. This distinction should be kept in mind by the treating physician. These states are similar but not identical.

Carlos G. Musso, MD Hospital Italiano de Buenos Aires - Argentina arlos.musso@hospitalitaliano.org.ar

Juan F. Macías Núñez, MD, PhD Hospital Universitario de Salamanca - Spain

Dimitrios G. Oreopoulos, MD, PhD Toronto Western Hospital - Canada


1) Coresh J, Astor B. Ann Internal Med. 2006; 145: 299-301

2) Musso CG. Geriatric nephrology and the "nephrogeriatric giants". Int Urol Nephrol 2002; 34(2): 255-6

3) Swartz R. Fluid, electrolyte, and acid-base changes during renal failure. In Kokko J, Tannen R (Eds). Fluids and electrolytes. Philadelphia. W.B. Saunders Company.1996: 487-532

4)Musso CG, Musso CAF, Joseph H, et al. Plasma erythropoietin levels in the oldest old. Int Urol Nephrol 2004; 36(2): 259-62

5)Wieczorowska-Tobis K, Mossakowska M, Niemir Z, et al. Wiad Lek. 2005; 56-61

6) Macías Núñez JF, Cameron S. Renal function in the elderly. In Cameron S (Ed). Oxford Textbook of Clinical Nephrology. Oxford. Oxford University Press. 2006

7) Rennke H, Denker B. Renal pathophysiology. Philadelphia. Lippincott Williams & Wilkins. 2007

8) Musso CG, Macías Nuñez JF. Renal physiology in the oldest old: the Sphinx remakes her question. Int Urol Nephrol. 200; 37(3): 653-4

9) Musso CG, Macías Núñez JF. Renal acidification, calcium, phosphate and magnesium. In Macías Núñez JF, Cameron S, Oreopoulos D (Eds). Renal ageing: health and disease. In press

10) Plantalech L, Knoblovits P, Cambiazzo E, et al. Hipovitaminosis D en ancianos institucionalizados de Buenos Aires. Medicina. 1997; 57: 29-35

11) Musso CG, Miguel R, Algranati L, et al. Renal potassium excretion: comparison between chronic renal disease patients and old people. Int Urol Nephrol 2005; 37(1): 167-70

12)Musso CG, Liakopoulos V, De Miguel R, et al. Transtubular potassium concentration gradient: comparison between healthy oldpeople and chronic renal failure patients. Int Urol Nephrol 2006; 38(2): 387-90

Conflict of Interest:

None declared

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