Showing posts with label Nephrology. Show all posts
Showing posts with label Nephrology. Show all posts

Monday, September 25, 2017

SIADH vs Diabetes Insipidus, Osmolarity and Sodium levels in urine and serum in both (mnemonic)

Serum and urine findings in SIADH and  Diabetes Insipidus can really mess up our brains :S

A nice mnemonic to memorize SIADH is to recall the letters as  :
 "S"odium "I"s "A"lways "D"own "H"ere (by here: I mean serum) =>
so in SIADH:
=> low Na in serum
=> high Na in Urine & high Urine Osmolarity

Now ...just think of the opposite and you ll get Diabetes Insipidus
so in DI:
=> high Na in serum /high serum osmolarity
=> low Na in Urine


Chronic Renal Failure : Indications for dialysis.

Hello guys!

In this post I am going to list down the Indications for dialysis in patients of Chronic Renal Failure.

Absolute Indications :
1. Volume overload not responding to medication.
2. Refractory hypertension.
3. Hyperkalemia unresponsive to medications.
4. Severe metabolic acidosis unresponsive to medications.
5. Uremic pericarditis
6. Neurological signs and symptoms of Uremia.
7. Plasma creatinine more than 1060 umol/l or BUN more than 36 mmol/l

Relative Indications :
1. Anorexia
2. Severe anemia unresponsive to erythropoietin.
3. Persistent severe pruritus.
4. Restless legs syndrome.

That's all.
Thank you

MD Mobarak Hussain (Maahii)

Friday, September 22, 2017

Renal stones and pH of urine mnemonic


Here's a post on the association between renal stones and pH of urine.

Which stones form in acidic urine?

Mnemonic: It's pretty simple, stones which have "weak acids" as a component.

Calcium oxalate (Oxalic ACID)
Cysteine (Which is an Amino ACID)

PS: This is just a mnemonic.

Which stones form in alkaline urine?

Calcium Phosphate
Magnesium Ammonium Phosphate

That's all!


Thursday, August 3, 2017

Causes of hematuria mnemonic

Hey Awesomites

Some common Glomerular causes of Hematuria:
( mnemonic: GH )
- Glomerulonephritis ( post infectious, membranoproliferative, rapid progressive, IgA nephropathy )
- Henoch- Schonlein nephritis

Non - glomerular causes of hematuria :
( mnemonic : HEMATURIa )
- Hemorrhage ( cystitis, PCKD )
- Allergic reaction ( interstitial nephritis )
- Trauma or Tumors
- Urinary tract infections / increased Urinary calcium 

Thats all
- Jaskunwar Singh 

Renal colic : Important points

Hey Awesomites

Some important points to be noted regarding renal colic:

Thursday, July 20, 2017

Oxalate stones in Crohn's Disease

A tricky Concept based question often asked in Medicine/Pathology MBBS Professional Exam-
Why Crohn's Disease patient often develop Kidney/Renal STONES, particularly OXALATE stones?

Tuesday, July 11, 2017

Pathophysiology of laboratory findings in tumor lysis syndrome

Which of the following electrolysi abnormalities will you see in tumor lysis syndrome?
Answer either high, normal or low for each of these - calcium, phosphate, potassium, uric acid.

Labs in tumor lysis syndrome -


When cancer cells lyse, they release potassium, phosphorus, and nucleic acids, which are metabolized into hypoxanthine, then xanthine, and finally uric acid. 

This leads to:

Hyperkalemia can cause serious — and occasionally fatal — dysrhythmias.

Hyperphosphatemia can cause secondary hypocalcemia, leading to neuromuscular irritability (tetany), dysrhythmia, and seizure, and can also precipitate as calcium phosphate crystals in various organs (e.g., the kidneys, where these crystals can cause acute kidney injury).

Uric acid can induce acute kidney injury not only by intrarenal crystallization but also by crystal-independent mechanisms, such as renal vaso-constriction, impaired autoregulation, decreased renal blood flow, oxidation, and inflammation.

Crystal-induced tissue injury occurs in the tumor lysis syndrome when calcium phosphate, uric acid, and xanthine precipitate in renal tubules and cause inflammation and obstruction.

That's all!


Type 2 RTA pathophysiology, notes and mnemonic

Hello! This post is on type 2 renal tubular acidosis.

What causes Type 2 RTA?
Defect in proximal bicarbonate reabsorption - resulting in a hypokalemic hyperchloremic metabolic acidosis.

The defect in proximal reabsorption of filtered HCO3-  in effect leads to decreased proximal NaCl reabsorption and a tendency for salt wasting. This causes hyperaldosteronism -  leading to increased K secretion by the distal nephrons.

Thursday, June 29, 2017

Greenish discoloration of Urine

The common causes of greenish discolouration of urine are :

(1) Phenol containing compounds: Promethazine, Propofol, Thymol,
(2) Dyes: Indigo-blue, Indigo carmine, Carbolic acid, Flavin derivatives,
(3 Biliverdin (in cases of long standing obstructive jaundice),
(4) Amitryptyline (anti-depressant),
(5) Pseudomonas infection,
(6) Cemetidine,
(7) Indomethacin,
(8) Methylene blue (bluish )

Saturday, June 24, 2017

Mnemonico diagnostico: Opacities that may be confused with renal calculus

Hey Awesomites

Mnemonic for opacities on a plain abdominal radiograph that may be confused with renal calculus:

Tubercular calcified lesions in the kidney
Ossified tip of 12th rib
Phleboliths (calcifications in the wall of pelvic veins)

Gall stones
Appendicular/ Adrenal gland concretions
Mesenteric lymph node calcifications
External (foreign) bodies in alimentary canal (ex., cyclopenthiazide)

Thats all
- Jaskunwar Singh

Wednesday, June 21, 2017

Hematuria: A clinical pearl

Hey Awesomites

Hematuria (blood in urine) may be microscopic or macroscopic/ gross.

The American Urological Association (AUA) defines microscopic hematuria as 3 red blood cells/ high - power field on microscopic examination of the centrifuged urine specimen in two of the three freshly voided, clean- catch, midstream urine samples.

Gross/ visible hematuria can result from as little as 1mL of blood in 1L of urine, and therefore, the color of urine does not necessarily reflect the degree of blood loss.

Now lets have a brief review of the clinical presentation of hematuria on the basis of its source -

- A glomerular source of bleeding (nephronal/ glomerular hematuria) usually results in persistent microscopic hematuria that may be with/ without intermittent periods of gross hematuria.

- Total hematuria (present throughout the void) indicates bleeding of bladder/ upper tract origin.

- If renal sources of hematuria are present, the blood is equally dispersed throughout the urine stream  and does not clot.

In cases of clotting, its localisation is a must to evaluate the underlying cause:

- Hematuria/ clots at the beginning of the urine stream ( initial hematuria ) is a symptom of a urethral cause.

Terminal hematuria occurring at the end of stream may be caused due to either prostatic, bladder, or trigonal source of bleeding.

Thats all
- Jaskunwar Singh

Sunday, June 18, 2017

Changes in glomerular dynamics mnemonic

Hello everyone!

If you forgot the afferent - efferent stuff from step 1, I have a mnemonic.

Remember ACE ID, PDA ANC.

Saturday, June 17, 2017

Effects of Angiotensin-II on GFR

So this is a highly confusing topic. No matter how many times you read it, some amount of doubt is always there in your mind. So an advice to the readers, bookmark this post because you will be needing to read it more than once to get the drift.

First of all, let us review the effects of Angiotensin II on Glomerulus.

It constricts both the afferent and efferent arterioles but preferentially increases efferent resistance. Why? 3 reasons:

1. Efferent arterioles have a smaller diameter in their basal state.

2. Ang II stimulates the release of vasodilator NO from the afferent arteriole.

3. Ang II minimizes vasoconstriction at the afferent arteriole via the stimulation of Ang II type 2 (AT-2) receptors, which result in vasodilatation through a CYP450 dependent pathway.

The net effect of preferential rise in efferent arteriolar resistance is that the glomerular pressure is increased or stabilized(in hypoperfusion states), which helps to maintain or increase GFR. But in the long run, lots of fluid have been filtered out leaving behind the proteins which raise the colloid osmotic pressure, eventually enough to overrule the hydrostatic pressure and hence it leads to decrease in GFR.

Ang II also reduces GFR by causing constriction of the mesangial cells which reduces the effective surface area for filtration. 


Saturday, June 10, 2017

Lowe syndrome mnemonic

Lowe Syndrome (Oculocerebrorenal dystrophy) mnemonic

Think of Lowe = Love and it'll make sense.

Lowe makes you blind (cataracts, glaucoma)

Lowe makes you HAPpy (High Alkaline Phosphatase along with normal calcium, low phosphate)

Lowe messes with your head (intellectual disability)

LoveR - Renal defects (proximal tubular acidosis, aminoaciduria, and low-molecular-weight proteinuria)

Lowes syndrome is a cause of Fanconi syndrome.

That's all!


Renal Cell Carcinoma Etiology : Summary

Hi everyone. Here's a short summary of the causes for Renal cell carcinoma !

Renal Cell Carcinoma ( or RCC) is a common tumor of the kidneys and is essentially an Adenocarcinoma.
It's quite often called as the 'great mimic' as it is relatively hard to diagnose.

Here's the list of causes of this tumor.

Remember :
CCCC or C4

C = Cigarette smoking and Tobacco usage.
C = Chronic Kidney Disease / Cystic (Acquired) Disease of kidneys.
C = Cadmium, Asbestos and other occupational Exposures.
C = Cancer Syndromes.
Important Cancer Syndromes =

- Von Hippel Lindau Syndrome :
3p mutation in VHL Gene which is a tumor suppressor --> Tumors seen include Cerebellar and Retinal Hemangioblastomas , Pheochromocytoma, RCC (Clear type) and various other Cystic tumors.

- Tuberous Sclerosis

- Birt Hogg Dube Syndrome : Associated with various weird skin changes and chromophobe type RCC.
Skin changes include --> Tumors of Hair disc (Tricho-discoma) , Tumors of Hair follicle - Fibrofolliculoma and Acrochordons ( skin tags).

- Hereditary Papillary Cancer : Associated with MET Gene mutations

- Hereditary Leiomyomatosis with RCC : Associated with multiple Fibroids in the uterus.

That's​ all for today!
Hope this helped.
Happy Studying !
And, as always , Stay awesome !

~ A.P.Burkholderia

Thursday, June 1, 2017

Pathophysiology of anorexia in chronic kidney disease

Normal appetite regulation: Appetite regulation involves the gastrointestinal tract (ghrelin as an appetite stimulant, and cholecystokinin, glucagon-like peptide-1, and neuropeptide YY as appetite inhibitors); the adipose tissue with leptin, a potent appetite inhibitor; the vagal system; and the brain, which integrates the stimuli in the hypothalamus area. Satiety relies on the melanocortin receptors with serotonin as the main neurotransmitter and is challenged with hunger peptides, namely, neuropeptide Y and agouti-related peptide.

What happens in CKD?

Thursday, May 18, 2017

Diabetes insipidus and water deprivation test

In this video I talk about pyschogenic polydipsia, central diabetes insipidus, nephrogenic diabetes inspidius, water deprivation test :)

Saturday, May 6, 2017

Acute Kidney Injury due to Anticancer drugs

Hey guys, there are multiple causes of acute kidney injury in a cancer patient, namely sepsis, metastasis, tumor lysis syndrome, etc. But there is another reason which we often overlook, which is drug-induced.

1. Thrombotic microangiopathy: Associated with agents targeting vascular endothelial growth factor(VEGF), eg., Ranibizumab, Bevacizumab. These drugs also block the angiogenesis in the glomerular vasculature, such that the injured endothelium isn't replaced, leading to multiple foci of platelet aggregations just like in TTP and HUS.

2. Focal segmental glomerulosclerosis: Associated with tyrosine kinase inhibitors are the most common and are frequently associated with acute kidney injury.

3. Acute Interstitial Nephritis:
The checkpoint inhibitors ipilimumab, nivolumab, and pembrolizumab activate host T cells to enhance tumor killing by preventing tumor ligand binding to cytotoxic T-lymphocyte antigen 4 and programmed death 1 receptors, which deactivate T cells. However, this effect causes loss of self-tolerance (and perhaps tolerance to other drugs), leading to various forms of autoimmune injury, including acute interstitial nephritis, which is associated with moderate-to-advanced-stage acute kidney injury.

That's all!


Friday, May 5, 2017

Uric acid and struvite stones mnemonic

Well, urine is largely water which *can* be considered as transparent. That's why, uric acid stones don't show up on X-rays.

Struvite or triple phosphate stones have Proteus has the causative factor. Remember p for p

That's all!

-Sushrut Dongargaonkar