Malnutrition-Inflammation Complex Syndrome: A Cause of Low Parathyroid Hormone in Patients With Chronic Kidney Disease

Rishi Raj,Aditya Kadiyala,Chinmay Patel

doi:10.7759/cureus.20324

Abstract

Secondary hyperparathyroidism is commonly seen in patients with chronic kidney disease (CKD) due to hypocalcemia, hyperphosphatemia and low vitamin D levels and is associated with high-turnover bone disease. In contrast, some patients with advanced CKD, including those requiring dialysis (end-stage renal disease [ESRD]), develop adynamic bone disease with features of low-turnover bone disease. Low serum parathyroid hormone (PTH) has been used as a biochemical marker of adynamic bone disease. Low PTH levels may not necessarily be due to adynamic bone disease but could be a manifestation of the malnutrition inflammation complex syndrome (MICS). The optimal management of hypoparathyroidism associated with MICS is not well known. Currently, there is insufficient evidence to suggest if there is any role in improving nutritional and inflammatory status among patients with CKD and MICS. Furthermore, it also remains unclear whether these changes will help address low PTH levels seen in these patients. We report three patients with advanced CKD who had very low PTH levels possibly attributed to MICS. In addition, we briefly discuss other characteristics and pathophysiology of MICS.

Highlights

Secondary hyperparathyroidism is common in patients with chronic kidney disease (CKD), and with decreasing estimated glomerular filtration rate (EGFR) levels, the majority of the patients (>80%) have parathyroid hormone (PTH) > 150 pg/mL [1]
We report three patients with advanced CKD who had very low PTH levels possibly attributed to malnutrition inflammation complex syndrome (MICS)
Adynamic bone disease (ABD) is a type of CKD-osteodystrophy commonly induced by overtreatment of secondary hyperparathyroidism, and its development reveals a deranged ability of uremic bone to maintain a normal bone turnover [1]

Summary

Introduction

Secondary hyperparathyroidism (serum PTH > 65 pg/mL) is common in patients with chronic kidney disease (CKD), and with decreasing estimated glomerular filtration rate (EGFR) levels, the majority of the patients (>80%) have PTH > 150 pg/mL [1]. A 51-year-old white female with a medical history of type 2 diabetes mellitus, obesity, hypertension, and low back pain was first evaluated by Nephrology in March 2015 for CKD stage 3a She was not a smoker and had no family history of kidney disease. This happened in the setting of poorly controlled diabetes, hypertension associated with nephrotic range proteinuria, and progressive CKD. As her creatinine and EGFR worsened, her PTH levels started trending down and remained suppressed despite low vitamin D levels. Reference range 11-17 mg/dL 70-110 mg/dL 8.3-10.4 mg/dL 3.5-5.0 mg/dL 0.60-1.10 mg/dL >60 mL/min/1.73m2 3.4-5.4 mg/dL 44-147 U/L 8.0-74.0 pg/mL 20-80 ng/mL

Discussion

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Conclusions

Disclosures