Find information on secondary hyperparathyroidism of renal origin, including clinical documentation tips, medical coding guidelines (ICD-10-CM N80.82), and healthcare resources. Learn about the diagnosis, treatment, and management of renal secondary hyperparathyroidism, including laboratory testing, phosphate binders, calcimimetics, and vitamin D analogs. Explore resources for healthcare professionals related to chronic kidney disease mineral and bone disorder (CKD-MBD) and its impact on parathyroid hormone (PTH) levels.
Also known as
Secondary hyperparathyroidism
Overactive parathyroid glands due to another condition.
Chronic kidney disease
Long-term kidney damage with progressive loss of function.
Disorders of mineral metabolism
Imbalances in minerals like calcium and phosphorus.
Atherosclerosis
Hardening and narrowing of the arteries due to plaque buildup.
Follow this step-by-step guide to choose the correct ICD-10 code.
Is the hyperparathyroidism secondary to chronic kidney disease?
Yes
Is the patient on dialysis?
No
Do NOT code E87.4. Review documentation for alternative cause and code appropriately.
When to use each related code
| Description |
|---|
| Secondary hyperparathyroidism renal |
| Primary hyperparathyroidism |
| Tertiary hyperparathyroidism |
Coding E88.8 (Secondary hyperparathyroidism) without specifying CKD stage (N75.1-N75.5) leads to inaccurate severity reflection and DRG assignment.
Failing to document the renal origin of secondary hyperparathyroidism can cause undercoding and missed MCC/CC capture impacting reimbursement.
Concurrent Vitamin D deficiency (E55.9) may be overlooked, affecting treatment plans and accurate reflection of patient complexity.
Q: What are the most effective management strategies for secondary hyperparathyroidism in patients with chronic kidney disease stage 5?
A: Managing secondary hyperparathyroidism (SHPT) in chronic kidney disease stage 5 (CKD-5) patients requires a multifaceted approach. Firstly, optimizing phosphate control with phosphate binders and dietary restriction is crucial. Secondly, calcimimetics, like cinacalcet or etelcalcet, can effectively lower parathyroid hormone (PTH) levels. Thirdly, vitamin D therapy, in the form of calcitriol or its analogs, can be beneficial, but requires careful monitoring of calcium and phosphorus levels. For refractory cases, parathyroidectomy remains an option. The choice of treatment depends on individual patient factors, including PTH levels, calcium and phosphorus balance, and presence of symptoms. Explore how combining these strategies can lead to improved outcomes in CKD-5 patients with SHPT. Consider implementing regular monitoring of PTH, calcium, phosphorus, and alkaline phosphatase to assess treatment efficacy.
Q: How do I differentiate between primary hyperparathyroidism and secondary hyperparathyroidism of renal origin based on laboratory findings and clinical presentation?
A: Differentiating primary hyperparathyroidism (PHPT) from secondary hyperparathyroidism of renal origin (SHPT) requires careful evaluation of laboratory findings and clinical presentation. In PHPT, serum calcium is typically elevated, while phosphate is often low or normal. PTH will be inappropriately elevated for the calcium level. Patients may present with symptoms related to hypercalcemia, such as kidney stones, bone pain, or gastrointestinal issues. In SHPT, the underlying chronic kidney disease leads to decreased phosphate excretion and reduced vitamin D synthesis. This results in hypocalcemia, hyperphosphatemia, and elevated PTH as a compensatory mechanism. Patients may experience symptoms related to renal osteodystrophy, such as bone pain and muscle weakness. Learn more about the nuanced differences in calcium, phosphorus, and vitamin D levels that help distinguish these conditions. Consider implementing a thorough patient history and physical exam to aid in accurate diagnosis.
Patient presents with signs and symptoms suggestive of secondary hyperparathyroidism of renal origin. The patient's chronic kidney disease stage [insert stage] is documented, contributing to mineral and bone disorder (CKD-MBD). Laboratory results reveal elevated parathyroid hormone (PTH) levels, along with abnormalities in calcium, phosphorus, and vitamin D metabolism. Specifically, the patient exhibits [specify elevated or decreased] serum calcium, [specify elevated or decreased] serum phosphorus, and low 25-hydroxyvitamin D levels. These findings are consistent with the diagnostic criteria for secondary hyperparathyroidism due to renal insufficiency. The patient's clinical presentation includes [document specific patient symptoms such as bone pain, muscle weakness, fatigue, pruritus, or other relevant symptoms]. Differential diagnoses considered include primary hyperparathyroidism and other causes of hypercalcemia. However, given the patient's established CKD, the elevated PTH in the context of abnormal calcium, phosphorus, and vitamin D levels, secondary hyperparathyroidism of renal origin is the most likely diagnosis. Treatment plan includes dietary phosphate restriction, phosphate binders as needed, calcimimetics if indicated per current guidelines (KDOQI, KDIGO), and vitamin D supplementation targeting optimal levels. Patient education regarding the management of secondary hyperparathyroidism in CKD and the importance of medication adherence was provided. Follow-up laboratory testing for PTH, calcium, phosphorus, and vitamin D is scheduled to monitor treatment response and adjust therapy as necessary. The patient's overall prognosis is linked to the management of their underlying CKD and the effectiveness of interventions to control secondary hyperparathyroidism.