Chronic kidney disease

 I HAVE BEEN GIVEN THIS CASE TO SOLVE IN AN ATTEMPT TO UNDERSTAND THE TOPIC OF ''PATIENT CLINICAL DATA ANALYSIS'' TO DEVELOP MY COMPETENCY IN READING AND COMPREHENDING CLINICAL DATA INCLUDING HISTORY,CLINICAL FINDINGS,INVESTIGATIONS AND COME UP WITH A DIAGNOSIS AND TREATMENT PLAN.

You can find entire real patient clinical problem by clicking this link here

1. ANATOMICAL DIAGNOSIS: chronic kidney disease complicated as Uremic cardiomyopathy.

    ETIOLOGIC DIAGNOSIS

        (a) Diabetic Mellitus: Albuminuria is an early indicator Diabetic glomerular disease.

            In diabetic patients presence of albuminuria is associated with increased cardiovascular mortality.

         (b) Hypertension.

2. REASONS FOR:

(a) AZOTEMIA: Fall in glomerular filtration rate and reduction in renal tubular secretory capacity prevent certain substances from being excreted by the kidney and these probably produce their adverse effects on every organ of the body. 

(b) ANEMIA:  

* Defeciency of erythropoietin 

* Toxic effects of Uremic on bone marrow precursor cells

* increased red cell distruction due to abnormal red cell membrane.

* deficiency of vit B12 and folate because of reduced dietary intake due to anorexia.

*blood loss during haemodialysis

(C)HYPOALBUMINEMIA:

*Massive protenuria decreases the serum albumin levels (Hypoalbunemia)

*Hypoalbuminemia decreases the colloid osmotic pressure of the blood resulting in disturbance in the starling forces acting across peripheral capillaries

*Hypovolemia also triggers the renin angiotensin aldosterone system which causes increase in absorption of Na and water by kidney resulting in edema

(D) ACIDOSIS:

*Impaired acid secretion in te late distal tubule 

*Impaired bicarbonate resorption in the Proximal tubule

* Impaired Na resorption in the late distal tubule 

3Q) Rationale for her treatment plan 

* TELMA (ARB) shouldn't have given on day 3 (bcz, creatinine is >3mg/dl)

*Why is she treated with tab.OROFOR even though her serum FE seemed withing normal limits.

* Why isn't she treated for hypocalcaemia and hyperphosphatemia since day 1

* Why Diet isn't followed since day 1.(like protein and salt restriction) and also there is no history regarding the patients diet here.

*Why isn't she treated for hypokalemia even when her pottasium levels started falling down.

* Why monocef was given (knowing it is a nephrotoxic drug).

* Why was the patient treated with sodium bicarbonate .

-sodium bicarbonate may be effective, but can cause edema and hypertension owing to extra cellular fluid expansion.

-calcium carbonate must have used.

-

4Q) -Dialysis therapy is urgently required if there is Hyperkalemia, rapid increase in creatinine, oliguria, severe metabolic acidosis.

- In our patient, on day 3 she developed SOB which might be due to pulmonary odema and that might be the reason for dialysis on day 3.

5Q)RISK FACTORS IN OUR PATIENT OTHER THAN DM AND HTN:

- family history of kidney disease

-Abnormal kidney structure

-Increased intake of nephrotoxic drugs

-obesity also might be the reason( investigations weren't done).

7Q)-Elevated central venous pressure potentially causes a decreased renal blood flow and renal perfusion pressure, and activates the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system, leading to a reduction in GFR.Additionally, higher central and renal venous pressure raises intrarenal interstitial pressures, leading to renal interstitial fibrosis and increased tubular pressure, further reducing GFR.

-Additionally increased, ventricular stiffness and arterial stiffness are commonly coupled in HFpEF patients, resulting in a system in which pressure and load changes are more dramatic, and may therefore negatively affect renal perfusion and function.

8Q) EFFICACIES OF PLACEBO OVER EPO

*ethically justifiable

*EPO is less effective in the prescence of iron deficiency, active inflamation and malignancy and patients with aluminium overload

* No side effects like headache, vomiting, bleeding

* No drug-drug interactions.

9Q) CKD-AQ 

The End-Stage Renal Disease-Adherence Questionnaire (ESRD-AQ) for patients requiring in-center HD was designed to measure treatment adherence behaviors in four dimensions: HD attendance, medication use, fluid restrictions, and diet recommendations. Items were initially generated based on in-depth literature reviews and in consultation with clinical experts, such as nephrologists and nephrology researchers, HD nurses, and renal dieticians. The final version of the ESRD-AQ consists of 46 questions/items divided into five sections. The first section pursues general information about patients' ESRD and RRT-related history (5 items), and the remaining four sections ask about treatment adherence to HD treatment (14 items), medications (9 items), fluid restrictions (10 items), and diet recommendations (8 items). These four final sections directly measure adherence behaviors (14, 17, 18, 26, 31, and 46), and patients' knowledge and perceptions about treatment (11, 12, 22, 23, 32, 33, 41, and 42). Responses to the ESRD-AQ utilize a combination of Likert scales and multiple choice, as well as “yes/no” answer format.

10Q) 

-Deficient protein intake results in the rapid loss of cellular ribonucleic acid and disaggregation of the endoplasmic reticulum–bound polysomes and, therefore, decreased albumin synthesis. Albumin synthesis can decrease by more than one third during a 24-hour fast. Albumin synthesis may be stimulated by amino acids produced in the urea cycle, such as ornithine.

-but, I don’t think her hypoalbuminemia is due to PEM.

                               CASE -2

https://bhavyayammanuru.blogspot.com/2020/09/aki-secondary-to-uti.html?m=1

Anatomical Diagnosis : acute kidney injury

DIFFERENCE BETWEEN AKI AND CKD:

(A)previous history of kidney disease is present in CKD( where as absent in AKI

(B)previous elevated creatinine >3 months in case of CKD(not in AKI)

(C)anemia is seen in CKD (but not in AKI)

(D)hypertension will be seen in CKD( And may or may not be in AKI)

(E)kidney is contracted in CKD(not In AKI)

(F) complications like hyperposphatemia,hypocalcemia,neuropathy,osteodystrophy,band keratopathy are seen in CKD and not in AKI.