Let’s start with a que
How do you define Hypercalcemia❓
Yup ❗❗U guessed it right ☑️
💥Hypercalcemia is total serum Ca+ > 10.5mg/dl and is classified as
🔆Mild: 10.5 to 11.9 mg/dL
🔆Moderate: 12.0 to 13.9 mg/dL
🔆Hypercalcemic crisis: > 14.0 aafp.org/afp/2003/0501/…
♨️Wait a minute
✳️Did u adjust the serum Ca levels (before correction) for serum albumin levels❓
💥Each 1 g/dL ⬇️serum albumin levels ↓⬇️ total Ca by approx 0.8 mg/dL
📣 Quiz time 🧐!!!!
🔥What is the most common cause of hypercalcemia❓
Your impression is probably correct ☑️
💥Approx 90% of all cases of ↑ Ca are caused by malignancy or HPTH
💥30% of cancer pt have ↑ Ca during the course
💥other causes r hypervitaminosis D, thiazides, renal failure, and rarely familial disorders.
what symptoms would u expect in pt of hypercalcemia❓
💦 Patients with mild hypercalcemia may be asymptomatic
💢Symptoms may vary from nonspecific N/V ⏭️ neurological such as confusion and even coma🧠 (when ⏫ Ca levels > 14 mg/dl).
💢 O/E may reveal
🌠CNS: confusion, paresis, hypotonia, Hyporeflexia
🌠GI: Fecal impaction (from constipation), Pancreatitis
🌠CVS: Arrhythmias
🌠Eyes👁️: Band keratopathy
🌠Signs of dehydration, kidney failure, malignancy
what is the mechanism of AKI in hypercalcemia❓
💥 AKI in ⏫ Ca can be due to
🌟Prerenal azotemia
🌟Direct vasoconstrictive effect on arteriolar smooth m/s
🌟⏬ glomerular ultrafiltration coefficient (Kf)
🌟Nephrocalcinosis/Nephrolithiasis
💥HD with ⏬Ca dialysate (≤1 mmol/L) is an effective measure in pts with acute ⬆️Ca, refractory to other therapies, and associated with significant AKI with oliguria and volume overload
💢 Now, let’s discuss role of steroids 🤔
✳️Useful in case of hematological malignancy and granulomatous disorders,
✳️MOA: Inhibit 1 a-hydroxylase, ↓ Ca absorption
Other rarely used agents :
💦Denosumab (Mab against RANKL)
❇️Useful in refractory and malignancy a/s ↑ Ca
No dose adjustment in Kidney failure, but monitor for low Ca
💦 Gallium nitrate ( in hypercalcemia of malignancy)
🔥 Can be nephrotoxic
SGLT2i 💊 are emerging as a promising agent to prevent and ⤵️the progression of DKD
Ever wondered
What do they do to electrolytes❓
Why r these diuretics not associated with electrolyte depletion❓
What is the impact of SGLT2i on Na and water hemostasis?
First, let’s revisit, how Na and glucose are handled in the nephron 📜
💥100% of the filtered glucose is reabsorbed along the nephron (90%, via SGLT2 in PCT)
💥1 Na+ ion for every glucose molecule gets absorbed from the lumen
💥In PCT 60 - 80% of sodium is reabsorbed