Bi weekly test.

 BIWEEKLY ASSESSMENT

1) What is your complete anatomic and etiologic diagnosis from the data available in the patient's online record linked above? (ignore the provisional diagnosis on admission mentioned in the case report)

In the context of patient symptoms(pedal edema & SOB& facial puffiness) anatomical diagnosis would be

? Kidney(albuminuria,microscopic hematuria)

?heart(pedal edema)

? Liver(no significant features suggesting hepatic dysfunction)

Etiological diagnosis

In the background of her diabetes I would suspect the ?early diabetic nephropathic changes which is rapidly progressing

I exclude hypertensive nephropathy because it is less likely to manifest with in one year of onset of diabetes

• Still considering the ?heart failure because of her pedal edema shortness of breath

I would exclude liver involvement because no evidence of hepatic dysfunction

2) What are the reasons for her:

Azotemia – may be due to precipitated AKI which I attribute to ?pre renal, ?intrensic renal failure

https://www.ncbi.nlm.nih.gov/books/NBK538145/

Anemia – ?may be due to decreased erythropoietin due to diabetic kidney disease leads to hypoproliferative anemia

Hypoalbuminemia – loss of podocytes whose membrane is negatively charged cannot repel negativity charged albumin that leads to albuminuria and hypoalbuminemia.

Acidosis - ?Renal failure leading to excess bicarbonate loss in urine leading to metabolic acidosis I excluded DKA because her GRBS was not markedly elevated

3) What was the rationale for her treatment plan detailed day wise in the record?

DAY1

1.inj.NaHCO3 100 meq/iv/stat in 100 ml NS = in view of sever acidosis & symptoms

2.syp.POTCHOLR 15 ml in one glass water tid = K+ supplementation because of hypokalemia.

3.w/h all OHA,anti hypertensives = to start on insulin for better glycemic control in hospital settings. Restriction of telmisartan was done because controversy of its use in patient with renal disease( enhances renal impairment)

DAY 2

1.inj.HAI according to sliding scale = to control sugars

2.t.PAN 40 mg od

3.inj.LASIX 40 mg iv bd if systolic bp >110mmhg to enhance urine output and reduce her edema

DAY 3

treatment-

1.inj.lasix 40mg iv bd decrease edema

2.tab.dytor 20mg of po decrease edema

3.inj.HAI S/C according to sliding scale controls sugars

4.tab.telma 40 mg od po->tab.nicardia 10 mg po/sos

Stopped telma

5.tab.orofer ct bd po

6.inj.erythropoietin s/c twice weekly = supplementation as on dialysis

7.tab.nodosis 500 mg bd po = to correct and prevent acidosis

8.tab.shelcal ct po/op calcium

9.syp.potcholr 15ml in one glass water tid = correct hypokalemia

4) What was the indication for dialysing her and what was the crucial factor that led to the decision to dialyze her on the third day of admission?

Dialysis indication in her = ?refractory Anuria despite giving lasix

                                                ?Refractory metabolic acidosis

                                             ? Worsening symptoms (sob due to fluid overload, tachypnoea due to acidosis)

Crucial factor = ? Worsening symptoms (sob due to fluid overload, tachypnoea due to acidosis)

                                  ?Refractory metabolic acidosis

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

?hypoalbuminemia beaches of albuminuria

?sepsis due to diabetic ulcer

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

https://cjasn.asnjournals.org/content/12/12/2032

May recover with residual renal function

?ESRD

Summary of risk factors by subgroupsa

Subgroup n Mean (Quartile Range: 25th to 75th Percentiles)

  UACR(g/g)b

Serum Creatinine(mg/dl) Serum Albumin(mg/dl) Hemoglobin(g/dl)

UACR (g/g)

    <2 1012 0.7 (0.4 to 1.2) 1.8 (1.5 to 2.1) 3.9 (3.7 to 4.1) 12.8 (11.5 to 14.1)

    ≥2 501 3.5 (2.6 to 4.5) 2.0 (1.6 to 2.4) 3.5 (3.2 to 3.8) 12.0 (10.7 to 13.1)

Serum creatinine (mg/dl)

    <2 965 1.0 (0.5 to 2.1) 1.6 (1.4 to 1.8) 3.8 (3.6 to 4.1) 12.9 (11.7 to 14.1)

    ≥2 548 1.6 (0.8 to 3.1) 2.4 (2.2 to 2.6) 3.7 (3.5 to 4.0) 11.9 (10.6 to 13.1)

• ↵a To convert UACR in mg/g to mg/mmol, multiply by 0.113; serum creatinine in mg/dl to μmol/L, multiply by 88.4; hemoglobin in g/dl to g/L, multiply by 10; and serum albumin in mg/dl to g/L, multiply by 10.

• ↵b Geometric mean for UACR.\

https://cjasn.asnjournals.org/content/1/4/761

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

Heart failure (HF) and chronic kidney disease (CKD) co-exist, and it is estimated that about 50% of HF patients suffer from CKD. Although studies have been performed on the association between CKD and HF with reduced ejection fraction (HFrEF), less is known about the link between CKD and heart failure with preserved ejection fraction (HFpEF).

3.1. Main Mechanisms for the Pathophysiology of CRS Type 2 Associated with Heart Failure and Normal Ejection Fraction (Table 1)

Table 1

Mechanisms thought to be involved in the pathogenesis of the cardiorenal syndrome in HFPEF patients.

Main mechanisms

(i) Intra-abdominal and central venous pressure elevation.

(ii) Activations of the renin-angiotensin systematic.

Other mechanisms

(i) Sympathetic overactivity.

(ii) Oxidative injury and endothelial dysfunction.

Precipitating factors

Disease conditions that is, Infections.

Drugs, that is, nonsteroidal inflammatory agents.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038429/

https://www.researchgate.net/figure/CONSORT-diagram-CARRESS-HF-indicates-Cardiorenal-Rescue-Study-in-Acute-Decompensated_fig1_329756008

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

recent large observational study found, for the first time, a reduction of mortality in transfused patients. However, most relevant clinical studies have methodological limitations suggesting that their results should be interpreted with caution.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782802/

9)What is the utility of tools like the CKD-AQ that assess the frequency, severity, and impact on daily activities of symptoms of anemia of CKD? Is Telegu among the 68 languages in which it is translated?

CKD and anemia questionnaire

The final CKD and Anemia Questionnaire (CKD-AQ) contains 23 items covering relevant symptoms and impacts associated with anemia of CKD (Table 6). The measure was translated into 68 languages to facilitate its use in global clinical trials. A conceptual framework for the final questionnaire is presented in Fig. 2. The questionnaire contains 8 items that assess the frequency of each symptom, all rated on a 5-point verbal rating scale. An additional 8 items assess the severity of these symptoms using an 11-point numerical rating scale. Five items assess the ability to do various activities, and 2 items assess the emotional impact of anemia of CKD.

Anaemia contributes to the impairment of health-related quality of life (HRQoL) in patients with CKD [7]. Its impact on patients’ HRQoL burden is exacerbated by reduced physical capacity and energy levels among these patients.

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 the evaluation of malnutrition in CRF patients?

Malnutrition is an important complication in CRI patients and ESRD patients on dialysis. SGA is a reliable method of assessing nutritional status. Most important is the fact that it can detect the changing trend of nutritional status, which may be missed by one-time anthropometry and biochemical methods.

11)this 58M had history of fever with cought and elevated tlc with indiacates renal acute kidney injury.As well there is no albuminuria,no edema

In 45M had had pedal edema ,facial piffiness,abdominal distention,anuria with clearly indicates nephrotic nephritic syndrome.and investigations showed that there is microalbuminuria,micro haematuria.Therapy in is patient

Etilogy of renal failure in 58M could be fever associated with cough which might have increased leucocyte count and caused renal aki


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