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The dialysis patient with a hidden inflammatory state: a quick clinical assessment.

Posted Mar 26 2010 12:00am
When caring for dialysis patients, we all use the well described KDOQI and KDIGO guidelines and ensure that the published goals are reached (please remember that the necessary government forms must also be completed!). We all pay special attention to the urea reduction ratio, the Kt/V, the PTH level and continuously test ourselves with the optimal management of “the uncontrolled hyperphosphatemic state". In addition to these markers and a physical examination (sometimes a forgotten cheap and valuable tool), I use a handful of specific laboratory tests which have helped me promptly determine the possible presence of a coexistent but hidden inflammatory state.

A reduced BUN/Creatinine ratio, an elevated total C02, a low uric acid level, a low Hb (specially if associated with a high ferritin level and a low reticulocyte count), a low cholesterol, a low phosphorus and a low albumin level are the ones which I have found to be most useful. In many outcome studies, several of these abnormalities have been found to be associated with increased mortality.


A
low BUN/Creatinine ratio (i.e. characterized by a ratio ≤ 10-15/1) usually implies a low urea generation rate as a result of protein-calorie malnutrition, suboptimal dialysis and/or liver disease.
An elevated or inappropriately normal predialysis bicarbonate level as well as a low uric acid usually denotes the presence of decreased net acid generation as a result of malnutrition.
Low phosphorus
, low cholesterol and/or low albumin levels are also seen as the result of malnutrition.
Resistance to the action of erythropoietic stimulating agents is usually suspected in the setting of an unresponsive anemia in conjunction with a hypo-proliferative bone marrow response (i.e. low reticulocyte index). This phenomenon can be the consequence of underdialysis, iron deficiency (as a result of decreased intake-administration, impaired utilization and/or increased losses) and endocrine dysfunction (e.g. hypothyroidism, uncontrolled secondary hyperparathyroidism).

In addition to the etiologies mentioned above, we should also consider (“think outside the box”) that any of them may also be caused by a common denominator – an inflammatory process. In addition to searching for an occult infection (particularly in patients with dialysis catheters), an ischemic skin ulceration, neoplasia, a clotting disorder, etc., we should also think of the retained clotted arteriovenous graft and/or the failed renal allograft as sources of malady! Clarification of their pathogenic role may not be easy as no clinical evidence of a problem (e.g. fever, renal allograft tenderness, hematuria, clotted AV graft warmth-erythema) may be noticeable (specially when patients returning to dialysis with a failed renal transplant are kept on “low dose prednisone”). Markers of inflammation such as an elevated ESR or CRP are useful but not specific. Nuclear studies using radiolabeled WBC’s and/or renal allograft biopsies are not only expensive-invasive but have not always being helpful. Therefore, we must always maintain a high index of suspicion and, if nothing else is found, we should remember that our friendly surgical colleague is just a phone call away!


Posted by Mario Rubin MD
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