Answer:

One of the things that jumps out with this patient is that they have some not-quite nephrotic range proteinuria and RBC casts when you spin their urine. In the context of a patient with worsening hypertension, vague systemic symptoms and worsening renal function, this is concerning for a nephritic syndrome. However, question of etiology becomes harder when you consider that hypertensive emergency can cause AKI, some proteinuria, RBC casts and RBCs on the UA. Is this patient presenting because they had a URI, overused sudafed, have undiagnosed OSA and poorly controlled hypertension? Or is this a systemic vasculitis?

A kidney biopsy in this patient can be a complex decision and it all depends on your pre-test probability. If your pre-test probability for this being a vasculitis is high, you would want to start steroids before a kidney biopsy, biopsy the patient as an inpatient, and send off a vasculitis serological work up. If your pre-test probability is lower, the patient has improved with blood pressure control and has a stable GFR, it is not unreasonable to send off a vasculitis work up and follow them up as an outpatient to monitor their kidney function and decide if a kidney biopsy is warranted.

The kidney is a highly vascular organ and is at high risk for bleeding. Optimizing this patient would involve getting their blood pressure < 140 systolic prior to biopsy and for the 24 hours after. One option is to try clonidine to try to control it orally, however as you run out of oral options or if the patient’s blood pressure is unpredictable a drip may be more useful. You could change this person from nifedipine to a nicardipine drip for better control peri-biopsy.

Great Review Article on Kidney Biopsy

Answer:

Since this is not a real rapid, we have time to wax and wane philosophical. Looking at the vitals, the patient is hypotensive with a narrow pulse pressure which points me away from etiologies of shock that cause vasodilation (neurogenic, septic) and more concerned about cardiac output (either due to pump failure or inadequate blood to pump). The patient is reflexively tachycardic, tachypneic and hypoxic.

The patient’s history of heart failure, CKD, and visible volume overload makes worry about cardiogenic shock - especially if the renal function is worsening quickly enough to warrant an inpatient renal biopsy. Has this patient ceased making urine and is now off the frank-starling curve? In the context of cardiogenic shock, pushing fluids could be dangerous unless they were for some reason pre-load dependent. It would help to touch the patient to see if they are cold or warm, and to talk to them to evaluate their mental status. The recent kidney biopsy is also very concerning for an RP bleed. Finally, the etiology for why the patient was getting a biopsy is important - nephrotic syndrome. Patient’s with nephrotic syndrome become hypercoagulable and should be anti-coagulated once their albumin < 2.5.

Looking at the ultrasounds from right to left: kidney - normal size, no hydronephrosis, and more importantly no signs of hematoma or RP bleeding; lung - good lung slide excluding tension pneumothorax, but he has several b-lines suggesting pulmonary edema; cardiac - this is the “D” sign, aptly named for the D-shape taken by the LV (normally circular) when RV overload occurs and there is paradoxical septal motion and flattening, as early diastolic RV pressure exceeds early diastolic LV pressure. This is a sign of RV strain.

This patient likely has a PE.

Answer:

This patient has both albuminuria and non-glomerular proteinuria, why?

There are four basic types of proteinuria - glomerular, tubular, overflow, and post-renal. Glomerular proteinuria is due to increased filtration of macromolecules (albumin) across the glomerular capillary wall. Albuminuria is a very sensitive measure of glomerular pathology. Tubular proteinuria is due to low-molecular-weight proteins (beta-2-microglobulin, light chains, etc) is due to small proteins that get normally filtered by the glomerulus, but do not get reabsorbed by the proximal tubule due to tubulointerstitial pathology. Overflow proteinuria is due to low-molecular weight proteins that are overproduced and overwhelm the capacity of the proximal tubules to reabsorb - almost always due to light-chains from multiple myeloma. These light chains can be toxic to the tubules and cause cast nephropathy. Post-renal proteinuria is poorly understood and can happen in the setting of infection.

This patient has a increase protein gap, worsening renal function, back pain and and proteinuria that is largely not glomerular - all these are concerning for multiple myeloma. MM can cause a number of different renal pathologies - immunoglobulin light chain (AL) amyloidosis and monoclonal immunoglobulin deposition disease (MIDD) causing glomerular damage and nephrotic syndrome, or light chain proximal tubulopathy and light chain nephropathy which can cause a faster worsening of GFR.

At this point, the patient should get a repeat renal panel with calcium, UA, UPEP/SPEP and this patient may need a kidney biopsy in the future.