Biiweekly assessment

1) diabetic kidney disease with anemia due to chronic kidney disease
 2).reasons for 
 • azotemia-elevated glucose levels  increase the speed of blood flow into the kidney, lowering the filtration time .
 • anemia- reduced erythropoietin levels 
Low EPO levels cause  red blood cell count to drop and anemia to develop.
 • hypoalbuminemia-changes in podocytes effacement cause albumin to filter leading to hypoalbuminemia
In glomeruli, there is mesangial expansion, thickening of the basement membrane, and, characteristically, nodular glomerulosclerosis
 • acidosis-Healthy kidneys remove acid from the body through urine and they keep the right amount of bicarbonate (base) in the blood. But in CKD, the kidneys can’t remove enough acid, which can lead to metabolic acidosis
For people with CKD, metabolic acidosis is defined as persistently low bicarbonate levels of less than 22 mEq/L in the blood.                         3) Rationale : syp potchlor was given because of the hypokalemia.. Inj. NaHCO3 was given because of metabolic acidosis ..Insulin and antihypertensives are given because known case of DM and HTN. Orofer XT was given because of anemia.. Inj. Lasix was given to decrease her volume overload. Spironolactone was given it was a potassium sparing diuretic.Calcium was given to the patient  because of hypocalcemia secondary to CKD. Indications of NaHCO3:metabolic acidosis in cardiac arrest, Tricyclic antidepressants, aspirin and phenobarbitone overdoses, Hyperkalemia, Crush injuries, C/I  in certain conditions because of adverse reactions like Hypernatremia, metabolic alkalosis, cellulitis, seizures, Tetany, sodium retention, peripheral edema.                    
   4) indication of dialysis in this pt: worsening of SOB secondary to metabolic acidosis with Anuria not resolved with high ceiling diuretics...                          
   5) Causes : primary : Minimal change disease, Focal segmental glomerulosclerosis, Membranous nephropathy.    
Secondary : DM, SLE, HIV , Viral hepatitis, malaria, amyloidosis,  Sarcoidosis, 
Drugs : Nsaids, gold, pencillamine Cancer: Hodgkin's and non Hodgkin's, solid tumours of GIT, RCC and lung.
6)Not all diabetics develop DN and in those who do, progression is variable. The main modifiable risks are hypertension, glycemic control, and dyslipidemia.
this patient might improve with few dialysis sessions or deteriorate to ESRD
7).2d echo,cardiac catheterization when pt develops  shortness of breath including exercise induced dyspnea, paroxysmal nocturnal dyspnea and orthopnea, exercise intolerance, fatigue, elevated jugular venous pressure, and edema.
comorbid conditions like diabetes cause a chronic inflammatory state releasing inflammatory mediators like
il6,TNF alpha->recruit the cells->fibrosis and hypertrophy-> diastolic dysfunction->heart failure with preserved ejection fraction
8) Mean hemoglobin levels, before and after study, in rHuEPO group were 8.85±1.01 g/dl and 9.90±0.29 g/dl, respectively (p<0.001) and in control group were, 9.00±0.09 g/dl and 7.81±0.23 g/dl, respectively
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293514/
9).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.)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 pt had a history of fever and no complaints of edema,
There were no signs Anemia
Investigations showed that there is elevated total counts and no microalbuminuria,microscopic hematuria, and the treatment given in this case was piptaz and amlong which were not the same in the other case

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