MEDICINE ONLINE ASSESSMENT

 A case of 45 year old lady with history of pedal edema which got progressed into abdominal distension and facial puffiness associated with decreased urine output,shortness of breath and chest pain on right side non radiating with intermittent palpitations.

Link to the above case:

https://alekyatummala.blogspot.com/2020/09/45-yr-female-with-anasarca.html?m=1

1)What is the complete anatomic and etiologic diagnosis from data available in patient's online record linked above?

ANATOMIC DIAGNOSIS:

Chronic kidney disease

ETIOLOGIC DIAGNOSIS:

Diabetic nephropathy

The disease progression in diabetic nephropathy involves various clinical stages:hyperfiltration,microalbuminuria ,macroalbuminuria,nephrotic proteinuria to progressive CKD leading to end stage renal disease.The damage is seen in all compartments of kidney:glomerulus,renal tubules,vasculature and interstitium.Renal fibrosis is the final common pathway of diabetic nephropathy.

Initially there is constriction of efferent arterioles and dilation of afferent arterioles with resulting glomerular hyperfiltration and glomerular capillary hypertension this gradually changes to hypofiltartion over time.Changes in the glomerulus include basement membrane thickening,widening of slit membranes of podocytes,increase in mesangial cells and matrix.This matrix invades capillaries and produces deposits called kimmelsteil wilson nodules,the cells and matrix completely expand and consume entire glomerulus shutting off the filtration.

https://en.wikipedia.org/wiki/Diabetic_nephropathy

https://www.grepmed.com/images/3123/pathophysiology-nephropathy-nephrology-diabetic-ckd

The other risk factors of CKD in this patient are hypertension and drugs she is used (query about use of NSAIDs,ACE inhibitors/ARBs should be made).

2)What are the reasons for her:

AZOTEMIA:Azotemia is an elevation of blood urea nitrogen and serum creatinine levels.Normally urea is reabsorbed from the tubules but creatinine is not reabsorbed therefore it approximately equals GFR.

Intrinsic/Intrarenal azotemia results from damage to kidney itself(glomeruli,tubules,interstitium and vasculature).This may result from vasculitis,toxins,drugs,infections and damage from hypoperfusion.

• BUN:creatinine ration<20:1
• FeNa>2
• Urine osmolality<300 mOsm/kg
• Urine analysis:cellular debris,muddy brown red cell casts and eosinophils may be seen,proteinuria is present.

BUN reflects only nitrogen content of urea(MW=28) and urea measurement reflects whole of molecule(MW=60).Urea is approximately twice that of BUN.

ANEMIA:

Causes of anemia in CKD are:

• Deficiency of erythropoeitin
• Toxic effects of uremia on bone marrow precursor cells
• Blood loss due to capillary fragility and poor platelet function
• Reduced intake,absorption and utilisation of dietary iron
• Anemia of chronic disease

HYPOALBUMINEMIA:

• Proteinuria
• Malnutrition
• Inflammatory status in poorly controlled diabetes mellitus
• Metabolic acidosis

ACIDOSIS:

Metabolic acidosis in this patient may be due to impaired ammonia excretion,reduced tubular bicarbonate reabsorption and insufficient renal bicarbonate production in relation to amount of acids synthesized by body and ingested with food.

https://link.springer.com/chapter/10.1007/978-1-84800-334-7_10

3)What was the rationale for her treatment plan detailed day wise in the record?Particularly mention rationale and efficacy for some drugs such as oral and iv bicarbonate?When is iv or oral bicarbonate indicated and why is contraindicated in certain situations?

• Inj.NaHCO3 is used to treat metabolic acidosis and to reduce tubulointerstistial inflammation.For mild acidosis usual dosage is 1 to 2 mEq/kg body weight administered slowly.For more severe acidosis 2 to 5 mEq/kg body weight may be used.Overdose may result in severe degree of alkalosis which may be treated by calcium gluconate or an acidifying agent.
• NaHCO3 is contraindicated in patients with hypocalcemia in which alkolosis may produce tetany.It is also contraindicted in excessive chloride loss and hypokalemia.
• Injection insulin according to sliding scale:How much insulin needs to be given to patient is decided based on her blood glucose levels.
• Inj.lasix is a loop diuretic for the treatment of oedema.
• Tab.orofer xt and Inj.erythropoeitin to treat the anemia.
• Oral syp.potchlor 15ml=20 mEq to treat mild-moderate hypokalemiaTreatment of acidosis with NaHCO3 may aggravate or precipitate hypokalemia due to intracellular shift of K+.Never give injection direct iv it can cause sudden hyperkalemia and instant death from cardiac arrest.
• Tab.telma and nicardia to treat her hypertension.
• Tab.shelcal for correction of secondary hyperparathyroidism.

4)What was the indication for dialysing her and what was the crucial factor that led to decision to dialyse her 

on day 3 of admission?

• Severe metabolic acidosis and refractory anuria.

5)What are the other factors other than DM and HTN that led to her current condition?

• Possible exposure to certain drugs like NSAIDs.
• Malnutrition and iron deficiency anemia.
• Older age.

6)What are the expected outcomes in this patient?Compare outcomes of similar patients globally and share your summary with reference links.

7)How and when would you evaluate her further for cardiorenal HFpEF and what are the mechanisms of HFpEF in diabetic renal failure patients?

In CKD risk factors for HF include long standing HTN with often worsened BP control as CKD progresses,salt and water retention causing excessive preload and cardiomyopathic factors including left ventricular hypertrophy and fibrosis.

https://www.ahajournals.org/doi/full/10.1161/circulationaha.116.022249

https://www.frontiersin.org/articles/10.3389/fphys.2019.01108/full

Diagnosis of cardiorenal HFpEF:

• Biomarkers for myocardial injury(troponin) and wall tension(BNP/NT-proBNP)
• Echocardiography

8)What are efficacies over placebo for available therapeutic options being provided to her for her anemia?

Anemia of chronic illness resulted in multiple blood transfusions in critically ill patients.This can be decreased with use of recombinant human erythropoietin therapy.It helped in achieving higher level of hemoglobin.

https://pubmed.ncbi.nlm.nih.gov/16878035/#:~:text=Recent%20data%20have%20shown%20that,their%20intensive%20care%20unit%20stay.&text=Main%20outcome%20measures%3A%20The%20primary,red%20blood%20cell%20units%20transfused.

Here is another study showing recombinant human erythropoeitin given subcutaneously is an effective and safe therapy in patoents in patients of anemia with CKD and who are not on dialysis.

https://www.sciencedirect.com/science/article/abs/pii/000293439090371J

9)What is the utility of tools like ckd-aq that assess frequency,severity and impact on daily activites of symptoms of anemia of ckd?Is telugu among the 68 languages in which it is translated?

CKD-AQ is a novel PRO(patient reported outcome)measure that captures frquency and severity of most relevant symptoms and impacts of anemia in CKD.

https://link.springer.com/article/10.1186/s41687-020-00215-8

The CKD-AQ went through linguistic validation into 71 languages ,30 of which were asia -pacific languages.

https://www.valueinhealthjournal.com/article/S1098-3015(18)35623-7/fulltext

10)What is the contribution of protein energy malnutrition to her severe hypoalbuminemia?What is the utility of tools such as SGA subjective global assessment in evaluation of malnutrition in CRF patients?

Nutritional assessment of patients in CKD is of vital importance.SGA is tool that uses 5 components of medical history (weight change,dietary intake,gastrointestinal symptoms,functional capacity,disease and its relation to nutritional requirements)and 3 componentsof brief physical examination (signs of fat and muscle wasting,nutrition-associated alternations in fluid balance) to assess nutritional status.

https://pubmed.ncbi.nlm.nih.gov/15483778/#:~:text=Subjective%20Global%20Assessment%20(SGA)%20is,fat%20and%20muscle%20wasting%2C%20nutrition%2D