https://www.facebook.com/496498187104262/

Dr.Tauqeer Nasir

Home
Pakistan
Swabi
Dr.Tauqeer Nasir

MBBS (KMU)
Registered GP – SCFHS, KSA
MCPS Medicine(CPSP)
FCPS Nephrology (CPSP)

Consultant Nephrologist & Transplant Physician by profession .

19/09/2025

Commonly Asked Question in Exam

Treatment of Hyperparathyroidism in CKD

Hyperparathyroidism in CKD is usually secondary hyperparathyroidism (due to phosphate retention, low vitamin D activation, hypocalcemia). Treatment aims at correcting the underlying biochemical abnormalities and protecting bone/vascular health.

1. Correct Hyperphosphatemia
• Dietary phosphate restriction (limit dairy, nuts, cola, processed foods).
• Phosphate binders (taken with meals):
• Calcium-based: calcium carbonate, calcium acetate (avoid if hypercalcemia).
• Non-calcium: sevelamer, lanthanum carbonate (preferred if hypercalcemia or vascular calcification).

2. Vitamin D Supplementation
• Vitamin D analogues (active form) to suppress PTH and correct hypocalcemia:
• Calcitriol, alfacalcidol, paricalcitol.
• Must monitor calcium and phosphate to avoid hypercalcemia/hyperphosphatemia.

3. Calcimimetics
• Cinacalcet, etelcalcetide → increase parathyroid calcium-sensing receptor sensitivity, lowering PTH.
• Especially used in dialysis patients with refractory hyperparathyroidism.

4. Parathyroidectomy
• Considered if:
• Severe secondary/tertiary hyperparathyroidism,
• Persistent very high PTH despite medical therapy,
• Complications: bone pain, pruritus, calciphylaxis, or soft tissue calcification.

Treatment Approach by CKD Stage
• CKD G3–G5 (non-dialysis) → control phosphate, correct vitamin D deficiency, monitor PTH.
• Dialysis patients → phosphate binders + vitamin D analogues ± calcimimetics.
• Refractory cases → parathyroidectomy.

18/09/2025

‏اگر یہ معاہدہ اسلام ، حرمین شریفین اور امت مسلمہ کے لیے ہے تو پاک فوج یہی والا فرض قبلہ اول بیت المقدس کے لیے کیوں پورا نہیں کرتی؟

12/09/2025

Crying alone... was the last thing she did 😥💔

04/09/2025

🩸 Erythropoietin Dosing – Anemia in CKD (Dialysis & Non-Dialysis)

✅ Starting Dose
IV or SC: 50–100 IU/kg, 3 times/week

🔄 Adjust Dose Based On Hemoglobin
📌 Check Hgb every 2–4 weeks
📈 If ↑ 1 g/dL in 2 weeks or Hgb >11 → Reduce dose by ≥25% or stop

🚫 Target Hgb: Stay ≤11 g/dL
Too high Hgb = ❗Risk of stroke, HTN, vascular events

01/09/2025

After completion of my MBBS from a recognised college I Got a decent job in CORPORATE hospital as a duty doctor

Under tremendous pressure from family to get married, I went to meet a girl under the arranged marriage system of India. After meeting girl rejected me upfront because she didn't liked my Job and of course I moved on and got married to another girl a year later.

After 5 years,
I saw the same beautiful lady at a traffic signal with her husband in a brand new Audi. And I was trying to kick start my hero Honda bike because the battery start was not working. She looked out of the car and briefly looked at me but without any hint of recognition due to helmet, she moves her eyes away!

At that moment, after riding a two wheeler for over 5 years, first time in my life I realized the value of a helmet
😂😂😂

So always wear a helmet in your own safety!

Issues in the public interest by an honest MBBS doctor

30/08/2025

🧪 Tumor Lysis Syndrome (TLS)

👨‍⚕️ Clinical Scenario:
A 48-year-old male was admitted to the ICU after receiving his first dose of chemotherapy for Burkitt lymphoma.
After 2 days, he developed:

Confusion

Oliguria (low urine output)

Tall T waves on ECG

Laboratory results:

Potassium: 6.8 mmol/L (⬆️)

Phosphate: high (⬆️)

Calcium: low (⬇️)

Uric acid: high (⬆️)

Creatinine: elevated (⬆️)

📌 Diagnosis: Tumor Lysis Syndrome (TLS)

---

📚 Definition

TLS is a life-threatening oncologic emergency caused by massive tumor cell lysis releasing intracellular ions and metabolites into the blood.

🧬 It commonly occurs after chemotherapy, especially in rapidly proliferating cancers like:

Burkitt lymphoma

Acute leukemias

---

🧠 Pathophysiology

Tumor cell lysis releases:

Potassium (K⁺) → Hyperkalemia → arrhythmia

Phosphate (PO₄³⁻) → binds calcium → Hypocalcemia

Nucleic acids → uric acid → Hyperuricemia → AKI

Creatinine rises due to kidney damage

---

🔍 Diagnosis – Cairo-Bishop Criteria

TLS = ≥ 2 lab abnormalities within 3 days before or 7 days after chemo:

Uric acid > 8 mg/dL

Potassium > 6 mmol/L

Phosphate > 1.45 mmol/L

Calcium < 1.75 mmol/L

Creatinine ↑ 1.5× baseline

OR: Arrhythmia or sudden death

---

🛡️ Risk Factors

High tumor burden

High proliferation (e.g., Burkitt, ALL)

High LDH

Pre-existing renal impairment

Chemo-sensitive tumors

---

🧰 Management

✅ Prevention (KEY)

💧 IV fluids (hydration)

🧂 Allopurinol (xanthine oxidase inhibitor)

💉 Rasburicase (high-risk or uric acid already high)

⚠️ If TLS develops:

1. 💧 Aggressive IV fluids: 2.5–3 L/m²/day

2. 💉 Rasburicase for uric acid control

3. 🧂 Hyperkalemia management:

Calcium gluconate (stabilizes myocardium)

Insulin + glucose (shifts K⁺ intracellular)

4. 💊 Phosphate binders

5. 🚫 Avoid calcium unless symptomatic hypocalcemia

6. 🏥 Dialysis if:

Refractory hyperkalemia/phosphatemia

Severe AKI

Volume overload

---

💡 Tips for Practice

Monitor K⁺, uric acid, phosphate, calcium daily after chemo in high-risk patients

Rasburicase works faster than allopurinol

Avoid NSAIDs, contrast — nephrotoxic

Early nephrology referral = better outcomes

---

✅ Key Takeaway:

Tumor lysis syndrome can be fatal if missed. Always think TLS in post-chemo patients with bulky tumors or lymphomas.

28/08/2025

CKD Therapeutic Landscape (2025)

CKD therapy has shifted from a single drug era (ACEi/ARB) to a multi-drug era (RAAS + SGLT2i + MRA, and soon GLP-1 RAs).

• The strategy is no longer just for diabetic kidney disease; it now applies to all CKD patients at risk of progression.

• By 2025+, CKD care looks more like heart failure care: combination therapy targeting different pathways for maximum kidney protection.

1. The foundation era (1990–2005): RAAS Blockade
• Trials like Captopril, IDNT, RENAAL, IRMA-2, MICRO-HOPE, REIN proved that ACE inhibitors and ARBs reduce proteinuria and slow CKD progression, especially in diabetic kidney disease (DKD).

• Key point: For almost 20 years, RAAS blockade was the only proven therapy for kidney protection.

2. The stagnation phase (2005–2014): No major breakthroughs
• Few new therapies emerged.
• Focus remained on blood pressure, glucose, and lipid control alongside RAAS inhibition.
• Clinical need: Additional drugs to further reduce CKD progression risk.

3. The revolution era (2015–2022): SGLT2 Inhibitors & MRAs
• CREDENCE (2019): First to show that SGLT2i (canagliflozin) protects the kidney independent of glucose control.
• DAPA-CKD (2020) & EMPA-KIDNEY (2022): Expanded benefits to non-diabetic CKD.

• SGLT2 inhibitors are now standard of care in CKD, not just in diabetes.

• FIDELIO-DKD & FIGARO-DKD (2020): Finerenone (non-steroidal MRA) showed added renal & CV benefit on top of ACEi/ARB.

• SONAR (2018): Endothelin receptor antagonists showed promise, though safety issues (fluid retention) limit use.

4. The expansion era (2023–2025 and beyond): New classes & broader populations
• FLOW trial (ongoing): Testing GLP-1 receptor agonist (semaglutide) for renal protection → may become the next big addition.
• FIND-CKD, ARTIC, PACIFIC, EASI-KIDNEY, ZENITH-HP: Investigating aldosterone synthase inhibitors, endothelin antagonists, SGLT2i combinations, and novel mechanisms in both diabetic and non-diabetic CKD.
• Trend: Trials now include patients with and without diabetes, making therapies more universal.

5. Clinical Practice Impact
• Past: Treat with ACEi/ARB only.
• Present (2025): Triple foundation therapy
RAAS blocker
SGLT2 inhibitor
Finerenone (in appropriate patients).

• Future: Likely quadruple therapy adding GLP-1 RAs or newer agents.

27/08/2025

Chinese researchers have successfully engineered a functional human kidney in vitro using stem cell–derived organoids seeded onto a biodegradable hydrogel scaffold. The construct developed organized nephron structures, including glomeruli, tubules, and urine-collecting ducts. When connected to an artificial perfusion system, the bioengineered kidney demonstrated physiological functions such as plasma filtration, urine production, electrolyte regulation, and hormonal responsiveness to antidiuretic hormone and aldosterone. Functional stability was maintained for over 60 hours under laboratory conditions. Current investigations are progressing in porcine models, with early-phase human clinical studies anticipated within two years. This advancement represents a significant milestone in regenerative medicine, with potential to provide patient-specific, rejection-free alternatives to kidney transplantation and dialysis.

25/08/2025

🩺 "Hypertensive Urgency" is now "Severe Hypertension" for BP >180/120 w/o target organ damage.

The 2025 AHA/ACC Hypertension Guidelines

23/08/2025

🔥👍

21/08/2025

🙂

18/08/2025

🌊 In response to the 2011 tsunami, Japan built a 395 km Great Tsunami Wall (up to 14.7m high, 25m deep) and planted 9 million trees as a “Great Forest Wall” 🌳—a blend of technology + nature for disaster safety.

🇯🇵 That’s their vision.
🇵🇰 And we? Still waiting for “relief funds” to reach the people…

Address

Swabi

Website

facebook.com

Alerts

Be the first to know and let us send you an email when Dr.Tauqeer Nasir posts news and promotions. Your email address will not be used for any other purpose, and you can unsubscribe at any time.

Contact The Practice

Send a message to Dr.Tauqeer Nasir:

Shortcuts

Want your practice to be the top-listed Clinic in Swabi?