MedKali MD

Medicine, politics and sports|MUHAS alumni

[MedKali MD @mexcellent90]

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[DJ KHALED @djkhaled]

GOD DID !

[CardiovascularCorner @TrackYourHeart]

ECG Leads That Localize Myocardial Infarction

[小谷祐樹 Yuki Kotani｜集中治療医 @YukiKotani5]

「重症患者での利尿薬について、最初に読みたい論文は？」
と聞かれたら、このBJAのレビューがオススメです。

ループに始まり、サイアザイド、アセタゾラミド、浸透圧利尿薬、K保持性利尿薬に至るまで、作用機序から実臨床での使い方まで一気にまとまった1本です。
https://t.co/GhmZjOs34O

[AJKD @AJKDonline]

Obesity in CKD: Core Curriculum 2026

https://t.co/zH9CjtaBwS (FREE)

@kramer_holly

[MedKali MD @mexcellent90]

@Doctors_GUILD Management of ascites due to liver cirrhosis

[Santiago Oquendo MD @rksanti]

🚨 LA ENFERMEDAD RENAL CRÓNICA (ERC) ya no debe diagnosticarse tarde. Un artículo reciente en Nephrology Dialysis Transplantation 2026 propone cambiar el paradigma: pasar de “tratar diálisis” a “PREVENIR ERC” 🩺🧠. El mensaje es contundente: una creatinina normal NO descarta daño renal ❌🧪, porque muchos pacientes ya tienen albuminuria elevada con TFG conservada 📉. La clave está en el enfoque ABCDE 🔍: A️⃣ Albuminuria, B️⃣ Presión arterial, C️⃣ Colesterol, D️⃣ Diabetes y E️⃣ eGFR. El gran problema actual es que la albuminuria sigue infrautilizada 📋, pese a que detectarla temprano permite iniciar nefroprotección con iSGLT2, IECA/ARA2, finerenona y agonistas GLP-1 💊❤️🩺, logrando retrasar diálisis incluso hasta 20–30 años ⏳. Además, esta revisión introduce un concepto revolucionario: “PRE-CKD” ⚠️, pacientes aún sin ERC formal pero con alto riesgo de desarrollarla, igual que ocurre con la prediabetes. El futuro de la nefrología será prevención, detección temprana y protección cardio-reno-metabólica 🌎🫀🧬. Pedir UACR anual en pacientes con HTA, DM2, obesidad o >60 años puede cambiar vidas. #CKD #ERC #Nefrología #Albuminuria #SGLT2 #Finerenona #PrevenciónRenal #CardioRenalMetabólico #KDIGO #MedicinaInterna

📚 Nephrol Dial Transplant. 2026;41:418–427. doi:10.1093/ndt/gfaf151.

[Gunnar Henrik Heine @gunnar_heine]

Obesity in CKD: Core Curriculum 2026
https://t.co/fA8MBqCpVw

[Leonardo Santos @Leo_Santo5]

🍬🏥Estrategias de Manejo de la Diabetes en Cuidados Críticos

🔰📚Med Clin N Am 2026

https://t.co/Bti1XZqDWT

Enlace a Articulo Completo👇🏻🆓✅
https://t.co/xumUMHaxVK

[Sociedad de Medicina de Emergencias de la Laguna @SOMELaguna]

🫘💧Diálisis Peritoneal en Lesión Renal Aguda

🔰📚Peritoneal Dialysis International

DOI: 10.1177/08968608251344356

Enlace a Artículo Completo👇🏻🆓✅
https://t.co/rPEDXf5xvO

[Jasmine Sethi @JasmineNephro]

🩸Anemia in CKD Management

https://t.co/MoQOpenBip

@NDTsocial

[Jasmine Sethi @JasmineNephro]

Coffee & CKD ☕🩺

Current evidence suggests moderate coffee intake is probably safe in CKD — and may even offer benefits

https://t.co/gdfPRPeAyN

@NDTsocial

[Jasmine Sethi @JasmineNephro]

🫘🧪Types of Proteinuria

UpToDate

[MedKali MD @mexcellent90]

@Neduszn8 Angel Di Maria, Sergio ramos and keylor Navas

[Dr Mmbaga @ZakayoMmbaga]

https://t.co/8oXHmJgyc2

Tumia link hapo juu kupata kitabu hiki kitakachokupa elimu kuhusu mtindo wa maisha magonjwa yasiyoambukiza kutoka Wizara ya Afya.

[Dr Ihab Suliman @IhabFathiSulima]

Acute Pulmonary Embolism (PE)
Key Finding
➤ McConnell’s Sign: Akinesia of the RV free wall with a hyperdynamic (sparing) apex.
Supporting Signs
➤ RV Dilatation: RV/LV ratio > 1.0.
➤ D-Shaped LV: Septal flattening due to RV pressure overload.
➤ 60/60 Sign: Pulmonary acceleration time < 60 ms + TR gradient < 60 mmHg.
Diagnosis
➤ Acute Massive/Submassive Pulmonary Embolism (PE).

[Leonardo Santos @Leo_Santo5]

Emergencias Metabólicas Relacionadas con el Alcohol🍺

💉Cetoacidosis
😵‍💫Wernicke-Korsakoff
🩸Hipoglucemia
🧂Hiponatremia

🔰📚Endocrinol Metab Clin 2026

https://t.co/y3cYZnkOOV

Enlace a Articulo Completo✅👇🏻🆓
https://t.co/xumUMHaxVK

[Sociedad de Medicina de Emergencias de la Laguna @SOMELaguna]

Análisis de Gases Sanguíneos 💉🩸

🔰📚MEDICINE International

DOI: 10.3892/mi.2025.291

Enlace a Artículo Completo👇🏻🆓✅
https://t.co/rPEDXf5xvO

[Cristobal Morales @CristobMorales]

https://t.co/sFRciVG2Ax REVIEW ARTICLE 1 April 26 @NEJM GLP-1 Receptor Agonists

[Dr. Chacón-Lozsán F .'. @franciscojlk]

💉DKA is not a glucose problem.
It’s a metabolic collapse.

We often simplify diabetic ketoacidosis as:

❌ “Severe hyperglycemia”

But that’s misleading.

👉 You can have normal glucose and still be in DKA

1. What really defines DKA

The classic triad:

Hyperglycemia

Anion gap metabolic acidosis

Ketonemia

But the key driver is:

👉 Insulin deficiency → unchecked ketogenesis

2. The dangerous trap: Euglycemic DKA

Up to ~3% of patients present with:

Glucose <250 mg/dL

Severe acidosis

High anion gap

-Common triggers:

SGLT2 inhibitors

Pregnancy

Starvation

👉 If you wait for hyperglycemia…
👉 You will miss it.

3. Think in triggers: the “5 I’s”

Infection

Infarction

Insulin (non-adherence)

Intoxication

Infant (pregnancy)

👉 DKA is always a consequence, not the disease itself.

4. The physiology most people forget

Total body potassium = LOW

Serum potassium = often NORMAL or HIGH

Why?

👉 Acidosis shifts K⁺ out of cells

Then you give insulin →
⚠️ Potassium crashes

5. The biggest treatment mistake

Stopping insulin too early.

👉 Insulin is NOT for glucose
👉 Insulin is for ketosis ⚠️

Never stop insulin until:

Anion gap closes

Bicarbonate normalizes

6. Fluids matter more than you think

Patients are often:

👉 4–6 liters depleted

And interestingly:

Balanced crystalloids may improve outcomes⚠️

Avoid hyperchloremic acidosis

7. The mindset shift

DKA management is not:

❌ “Lower glucose”

It is:

✅ Stop ketogenesis
✅ Restore volume
✅ Correct electrolytes
✅ Treat the trigger

🤓Final message

If you remember only one thing:

👉 Normal glucose does NOT exclude DKA

📃Reference
Lowie BJ. Endocrinol Metab Clin N Am 55 (2026) 1–10 https://t.co/Vr8jKaeQJt

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫨HHS is not just “very high glucose.”
It’s a dehydration-driven neurological emergency.

We often compare it to DKA…
But the physiology is completely different.

👉 And missing that difference can be dangerous.

1. What defines HHS

Not ketones. Not acidosis.

👉 Hyperosmolarity + neurologic dysfunction

Glucose >600 mg/dL

Osmolality >320 mOsm/kg

Altered mental status

Minimal or absent ketosis

2. The key difference vs DKA

DKA → insulin deficiency → ketosis

HHS → relative insulin → NO ketosis

👉 Enough insulin to suppress lipolysis
👉 Not enough to control glucose

3. The real problem: WATER LOSS

This is what kills the patient.

👉 Volume deficit can reach up to 9 liters

Mechanism:

Hyperglycemia → osmotic diuresis

Free water loss > sodium loss

Rising osmolality → brain dysfunction

👉 It’s a spiral of dehydration → hyperglycemia → more dehydration

4. Why patients present late

HHS develops:

👉 Days to weeks

Not hours like DKA.

So patients arrive with:

Severe dehydration

Confusion / coma

Often elderly, frail, or septic

5. The biggest management mistake

Starting insulin too early.

❌ Treating it like DKA

👉 In HHS, first step is:

FLUIDS. LOTS OF FLUIDS.

1–1.5 L in first hour

Then guided resuscitation

Only after:

✅ Volume restored
✅ Electrolytes checked

→ Then insulin

6. The hidden danger

Lowering glucose too fast.

👉 Rapid drop in osmolality
👉 Water shifts into brain

⚠️ Cerebral edema

Target:

↓ glucose by 50–75 mg/dL/hour

Maintain ~250–300 mg/dL initially

7. Always search for the trigger

HHS is rarely spontaneous.

Common causes:

Infection (most common)

MI / stroke

Dehydration

Medication non-adherence

🤓Final message

If DKA is a metabolic emergency…

👉 HHS is a hemodynamic + neurological emergency

And the treatment priority reflects that.

📃Reference
Lovegrove SS, Endocrinol Metab Clin N Am 55 (2026) 11–20 https://t.co/LoW1AnyKSk

[Abdulla A. Damluji, MD, PhD @DrDamluji]

Discontinuation of Beta-Blocker Therapy after Myocardial Infarction: @NEJM

🥸 SMART-DECISION: more on beta blockers discontinuation!

😱 Keep reading

👇👇👇