Everything You Need To Know About Diabetic Nephropathy

Get ready to scale up your Medicine preparation with this super informative blog post on Diabetic Nephropathy. 

In this blog post, you will learn everything you need to know about Diabetic Nephropathy including what it is, how and why it develops in patients, the causes leading to it, histopathological aspects and its treatment

And best of all, it will help you get an edge in your NEET PG exam preparation. 

Introduction

• Most common cause of C.K.D (chronic kidney disease)
• Most common indication of Kidney Transplantation
• Occurrence depends on Duration of disease and Severity of the disease
• Type 1 DM (HbA₁C > 7%) for more than 5years leads to nephropathy
• And in Type 2 DM more than 20 years leads to nephropathy
• Bilateral enlarged kidneys 
• Other conditions where bilateral enlarged kidneys are seen include
  • HIV associated Nephropathy
  • Amyloidosis
  • Diabetes Mellitus
  • Polycystic kidney disease
  • Hydronephrosis
• Painful unilateral enlarged kidney with Acute kidney Injury: Renal vein Thrombosis

Screening

• Albumin Excretion Rate or Urine Albumin creatinine Ratio
  • In Spot urine sample we check for Urinary Albumin Creatinine Ratio
    • Spot sample = Albumin (mg)/Urinary Creatinine (gm)
  • 30-300 mg/gm (moderately increased albuminuria): increase in cardiovascular mortality
  • Serum creatinine may be Normal
    • Rises late (After 60% of kidney damaged)
    • Most specific: Kidney function test
• Low dose ACE inhibitors or ARB can reduce the progression of disease

Histopathological aspect of Diabetic nephropathy 

Diffused glomerular sclerosis: Most common histopathological finding seen in a patient of Diabetic nephropathy

• Nodular glomerulosclerosis: Kimmelstiel Wilson Change
• Armani Ebstein change: Affects PCT
• Damage to DCT leads to development of Type – 4 RTA (Renal tubular acidosis)
  • In RTA 4, Aldosterone Resistance > Aldosterone deficiency
  • Thus ENaC (Epithelial sodium channel) become defective resulting in aldosterone resistance, Impaired excretion of K⁺/ H⁺

Medicine related articles:

GFR in Diabetic Nephropathy

• Initial 0-5 years there will be GFR increased: Glomerular hyperfiltration
• 5-10 years → Albuminuria → Irreversible damage.
• False positive albuminuria:
  • Hypertension 
  • Congestive Heart Failure 
  • Pyelonephritis
• Co-existing: Complications in DM at onset of Albuminuria
  • HTN
  • Non healing ulcer
  • Peripheral Vaso-occlusive disease

Treatment

• Stop Metformin / Sulfonylurea: GFR < 30 ml/min

Initiate Insulin: 80% of calculated dose

Target BP  

• < 130/80 mm of Hg if Tolerated
• ACE Inhibitor / ARB
• Side effect: Hyperkalemia (due to Type IV RTA)
• If K⁺ is increasing the stop ACE inhibitors and start CCB
• If Potassium is not rising and BP is not under control the combination of ACE + CCB can be given, if edema present then add thiazide
  • If eGFR <30ml then the diuretic used: metazolone
• In ESRD patient, K+ is increasing then Alpha blockers are used

Treatment of Hyperkalemia

• K⁺ Binding Resins - Sodium polystyrene sulfate
• Patiromer
• Sodium Zirconate

Transplant indication

• eGFR < 20 ml/min/ 1.73 m²

Also Read: EPILEPSY AND Electroencephalography (EEG) : NEET PG Medicine

Q. A chronic renal insufficiency patient present with peripheral edema and reduced urine output. Which of the following drugs will be suited in this patient for management of high renin Hypertension?

A. Aliskiren

B. Chlorthalidone

C. Prazosin

D. Beta blocker

We hope this article has helped you understand Diabetic Nephropathy for Medicine preparation. For more such information, download the PrepLadder app and study with the Dream Team Next Edition (India’s top Medical faculty).